MicroRNAs in psoriasis and psoriatic arthritis: a narrative review of potential diagnostics and current challenges

Introduction

Psoriasis (PsO) is a common chronic inflammatory disease caused by a complex interaction between genetic, environmental, and immunological factors, affecting 0.51% to 11.43% of the global adult population (1). It presents in distinct clinical forms, and chronic plaque PsO (or PsO vulgaris) is the most common, occurring in approximately 85–90% of cases (2-4). This pathology typically presents symmetrical erythematous plaques with silvery scales on the scalp, elbows, knees, and lower back (4).

The severity of PsO can vary widely, from mild forms characterized by a few localized inflammatory lesions to more severe cases with extensive plaques affecting more than 10% of the body surface area (5). Other less common subtypes of PsO include erythrodermic, pustular, guttate, inverse, and palmoplantar forms, each presenting distinct morphological and clinical characteristics (5). Psoriatic arthritis (PsA) is a chronic, long-term inflammatory musculoskeletal disease that affects approximately 20% to 30% of individuals with PsO (6,7). This chronicity underscores the long-term impact and challenges of the disease. PsA can develop at any stage of PsO, although it most commonly manifests, on average, about a decade after the onset of skin symptoms (8).

PsA is characterized by a broad spectrum of musculoskeletal manifestations, including arthritis, enthesitis, dactylitis, and axial involvement (9). Furthermore, non-musculoskeletal features are also present, such as skin and nail diseases, uveitis, metabolic syndrome, cardiovascular diseases, psychological comorbidities, among others (9). Collectively, PsO and PsA are referred to as “psoriatic disease”, which, when occurring independently or together, significantly impairs quality of life and requires appropriate treatment (9).

The diagnosis of PsO and PsA is currently based on clinical findings and symptoms. To aid in a more accurate diagnosis of PsO, the Psoriasis Area and Severity Index (PASI) acts as an indicator of disease severity and treatment monitoring (10). For PsA, several classification criteria have been developed to aid both clinical research and routine rheumatological practice, with the Classification Criteria for Psoriatic Arthritis (CASPAR) criteria being the most widely adopted (11). However, the often non-specific clinical presentation of PsA poses significant diagnostic challenges for healthcare professionals caring for patients with PsO. It is estimated that approximately 10% to 15% of individuals with cutaneous PsO have undiagnosed PsA (12). Since delays in diagnosis are associated with worse radiographic outcomes and greater functional impairment, identifying new biomarkers for the early diagnosis of this condition is highly desirable.

In this context, microRNAs (miRNAs), which are small non-coding RNA molecules involved in post-transcriptional regulation, have emerged as potential candidates. They are involved in various biological processes, including angiogenesis, immune cell activation, cell motility, and apoptosis (13,14). Although abnormal miRNA expression has been well-documented in several autoimmune diseases (15), the specific role of miRNA in the pathogenesis and diagnosis of PsO and PsA remains poorly understood.

MiRNAs are ~22-nucleotide non-coding RNAs generated through a conserved biogenesis pathway involving Drosha, DGCR8, Exportin-5, and Dicer, culminating in the assembly of the RNA-induced silencing complex (16-21). Through post-transcriptional repression of multiple target mRNAs, miRNAs regulate a broad spectrum of biological processes, including immune cell activation, cytokine production, keratinocyte proliferation, apoptosis, and tissue remodeling (22-28). MiRNAs are key regulators of cellular and immune homeostasis, controlling proliferation, apoptosis, and gene expression, and shaping both innate and adaptive immune responses (29,30). Dysregulation of miRNAs such as miR-155 and miR-146a contributes to aberrant inflammation and is implicated in autoimmune diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus, and PsO (15,18,29-33). Acting through pro- and anti-inflammatory pathways, miRNAs influence immune-cell activation, cytokine production, and tissue repair mechanisms (30,31,34,35). Because inflammatory processes often alter miRNA expression and processing, their modulation significantly affects transcription factors and mediators that drive chronic inflammatory disease, highlighting their relevance as central regulators of inflammation and tissue homeostasis.

Recent reviews have examined miRNAs in psoriatic disease; however, most have focused either on general inflammatory pathways or on PsO alone, without comparing cutaneous and articular phenotypes. Existing review articles also fail to fully integrate findings from diverse biological samples, such as peripheral blood mononuclear cells (PBMCs), serum, plasma, and extracellular vesicles (EVs), nor critically assess their discriminatory power in distinguishing PsO from PsA. Therefore, an up-to-date synthesis specifically addressing differential miRNA expression between PsO and PsA, and its potential utility in predicting progression from skin-limited disease to PsA, remains lacking.

Therefore, this study presents key information regarding circulating miRNA levels in patients with PsO and PsA, evaluating their potential as biomarkers in differentiating these conditions and predicting the progression of PsO to the articular phenotype. We present this article in accordance with the Narrative Review reporting checklist (available at https://jlpm.amegroups.com/article/view/10.21037/jlpm-25-38/rc).

Methods

This study, a narrative literature review, was conducted to present and critically analyze the available evidence on differentially expressed miRNAs in patients with PsO and PsA. The review followed the following steps: defining the topic and formulating the research question, establishing inclusion and exclusion criteria, searching and selecting articles in databases, and extracting and analyzing relevant data. The search was conducted in the PubMed and Web of Science databases, using the descriptors “psoriasis”, “psoriatic arthritis”, and “microRNA” combined with the Boolean operator “AND”. Studies published in English, available in full text, and covering all studies published from 2010 to April 2025 were included.

The inclusion criteria included original experimental articles that investigated the influence of genetic variants on miRNAs and the expression of miRNAs in human biological samples, such as serum, plasma, EVs, or PBMCs, in patients with PsO and/or PsA. Studies that included healthy control groups or patients with other rheumatological diseases, such as RA and ankylosing spondylitis, aiming to compare miRNA expression profiles, were also considered eligible. Studies that used bioinformatics analyses, when their results were compared and associated with biological samples, were also used in the study. Review articles, duplicate articles, studies based exclusively on secondary data analysis, in vitro studies with isolated cell cultures, and research conducted exclusively in animal models without any validation in human biological samples were excluded. The summarized strategy is presented in Table 1.

Results

Based on an understanding of the general mechanisms of miRNA biogenesis and action, as well as their roles in regulating inflammation and tissue homeostasis, we identified 30 articles in the PubMed database and 20 in the Web of Science. After screening and applying the inclusion criteria, 17 studies with similar clinical designs were selected for further analysis. Table 2 summarizes the included studies, the miRNAs differentially expressed between the two diseases, and their key reported findings. In addition, a summary flowchart describing the ideal workflow for the discovery, validation, and clinical translation of miRNA biomarkers is shown in Figure 1.

Figure 1 A summary flowchart describing the ideal workflow for the discovery, validation, and clinical translation of miRNA biomarkers. Key challenges and potential solutions at each stage are highlighted. CASPAR, Classification Criteria for Psoriatic Arthritis; DAPSA, disease activity in psoriatic arthritis; EVs, extracellular vesicles; MIQE, Minimum Information for Publication of Quantitative Real-Time PCR Experiments; miRNA, microRNA; NGS, next-generation sequencing; PASI, Psoriasis Area and Severity Index; PBMCs, peripheral blood mononuclear cells; PsA, psoriatic arthritis; PsO, psoriasis; RT-qPCR, reverse transcription quantitative polymerase chain reaction.

Discussion

MiRNAs and their association with PsO and PsA

Complex and incompletely understood mechanisms characterize PsO. A central feature is the aberrant activation of the adaptive immune system, involving T-helper 1 cells (TH1)- and T-helper 17 cells (TH17)-driven cytokine responses such as tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), interleukin (IL)-23, IL-17, and IL-22, as well as upregulation of intercellular adhesion molecule 1 (ICAM-1) (52). These mediators promote keratinocyte hyperproliferation, angiogenesis, and tissue infiltration, resulting in psoriatic plaque formation (4). Genetic susceptibility also contributes meaningfully, including HLA-Cw6, HLA-DQ*02:01, CCHCR1, CYP1A1 alleles and loci such as PSORS1-9 and PSORSASI (53). MiRNAs expressed in skin and immune cells modulate epithelial differentiation, keratinocyte proliferation, and inflammatory signaling, reinforcing their biological relevance (54). PsA, which affects ~20% of PsO patients, likewise presents several miRNA-linked inflammatory signatures, though many remain insufficiently defined (6). The main immunological and cellular pathways involved in the pathogenesis of PsO and PsA are shown in Figure 2.

Figure 2 Main immunological and cellular pathways involved in the pathogenesis of psoriasis and psoriatic arthritis. The diagram summarizes the main pathogenic axes involved in PsO and PsA. Activation of dendritic cells, macrophages, and keratinocytes triggers an inflammatory circuit sustained by IL-23/IL-17, TNF-α, and IFN-γ pathways, promoting epidermal proliferation, neutrophil recruitment, and lymphocyte infiltration. In PsA, the interaction between immune cells and the bone microenvironment stimulates osteoclastogenesis via RANK/RANKL, contributing to joint damage. The figure highlights the overlap and biological particularities of the two psoriatic disease phenotypes. IL, interleukin; IFN-γ, interferon gamma; IRAK1, interleukin-1 receptor-associated kinase 1; miRNA, microRNA; NF-κB, nuclear factor kappa B; PsA, psoriatic arthritis; PsO, psoriasis; RAN, receptor activator of NF-κB; RANKL, receptor activator of NF-κB ligand; TLR, Toll-like receptor; TNF-α, tumor necrosis factor alpha; TRAF6, TNF receptor-associated factor 6.

Circulating miRNAs with diagnostic potential for distinguishing PsO from PsA

MiR-92a-3p and related biomarkers

Characterization of circulating miRNAs in different biological matrices has revealed signatures capable of distinguishing PsO and PsA. Among the most consistent findings, miR-92a-3p, miR-19b-3p, let-7b-5p, and miR-21-5p stand out, with miR-92a-3p being the most promising candidate (36). Reduced expression of miR-92a-3p was subsequently confirmed in PBMCs from patients with active PsA (37), corroborating systemic downregulation during inflammatory exacerbation. Interestingly, miR-92a-3p demonstrates a specific disease context. In other contexts, it is overexpressed, promoting osteoblastic differentiation and bone regeneration (55), serving as a prognostic marker in colorectal cancer (56) and correlating with the progression of chronic kidney disease (57). These divergent profiles highlight the need to interpret miR-92a-3p expression within disease-specific regulatory networks, rather than as a universal biomarker.

MiRNAs implicated in the active and remission phases of PsA

MiR-126-3p and miRNA signatures of active disease

The miR-126-3p exhibits disease phase-dependent behavior. It is downregulated during active PsA and upregulated during remission. Functional analyses indicate that miR-126-3p downregulates inflammation- and bone-remodeling genes, including SPP1, AKT2, RANKL, and SDC2, establishing a direct role in the pathophysiology of PsA (37). Other miRNAs reduced during active PsA include miR-130a-3p, miR-148a-3p, miR-151a-5p, miR-192-5p, miR-199a-3p, and miR-17-5p, each converging on TNF, mitogen-activated protein kinase (MAPK), WNT, and proteoglycan pathways (37). These molecular disturbances align with the known inflammatory architecture of PsO and PsA, in which innate and adaptive immune activation drives cytokine cascades involving TNF-α, IFN-γ, IL-17, IL-22, and IL-23 (52). Consistent with this profile, elevated concentrations of TNF-α, IL-1, IL-1β, and IL-6 have been documented in both psoriatic skin and synovial tissue of PsA patients with peripheral joint involvement (9), reinforcing the continuity between cutaneous and articular inflammation. Articular manifestations generally follow cutaneous disease in approximately 75% of patients, although 10–15% develop PsA before or simultaneously with PsO (58), highlighting the need for early and reliable molecular biomarkers.

Differential miRNA expression between PsA and other arthritis

MiR-140 and miR-181b as cross-disease discriminators

A study comparing PBMC miRNAs across PsA and RA observed significantly increased miR-140 levels in PsA and reduced levels in RA (38). MiR-140 and miR-181b were both upregulated in PsA, whereas miR-21, miR-223, and let-7e appeared lower relative to RA. MiR-140 is well characterized in chondrocyte biology and joint homeostasis (38,59,60) and has also been proposed as a biomarker in osteoarthritis (61). It is downregulated in RA synovial tissue and fluid (62) and regulates vascular endothelial growth factor (VEGF), insulin-like growth factor (IGF), and transforming growth factor beta (TGF-β) receptor signaling (63-65). Although direct evidence of its involvement in PsO is still limited, these mechanistic pathways intersect with psoriatic inflammation, supporting the rationale for comparative miR-140 profiling between PsO and PsA, particularly PsA without cutaneous involvement (38).

EV-derived miRNAs as emerging biomarkers

Two miRNAs contained in EVs, miR-let-7b-5p and miR-30e-5p, were consistently lower in PsA than PsO, correlating robustly within the PsA cohort (39). Their circulating abundance is inversely associated with PsA even after adjustment for clinical confounders, with area under the curve (AUC) values of 0.68 and 0.69, respectively. Notably, the discriminatory capacity of miR-let-7b-5p is supported by independent evidence linking its reduced levels to magnetic resonance imaging (MRI)-detected tenosynovitis in PsA (36), reinforcing its potential relevance in entheseal and tendon-related pathology. MiR-let-7b-5p exerts context-dependent functions, activating TLR7-dependent inflammatory pathways in some settings (66) while providing anti-atherogenic protection in others (67). Its downregulation in PsA may reflect perturbations in IL-6, HMGA1/2 (68,69), and PRDM1 (70,71) regulatory networks, all of which are implicated in osteoclastogenesis and chronic inflammation. Conversely, miR-30e-5p, a negative regulator of BMI1 (72,73) and LRP6 (74,75), also shows decreased abundance with increasing PsA severity, suggesting that the loss of this miRNA may weaken protective mechanisms related to bone and immune homeostasis (39).

Serum EV miRNAs in PsO vs. PsA

Another EV-focused study reported increased levels of miR-423-5p, miR-335-5p, and miR-342-3p in PsO, alongside reduced miR-99b-5p (40), a miRNA previously linked to keratinocyte hyperproliferation. miR-10a-5p and miR-34a-5p, overexpressed in osteoarthritis, similarly contribute to cartilage degradation (76,77). Between PsA and PsO vulgaris, miR-671-3p was reduced in PsA, associating with cartilage breakdown. MiR-33a-5p, miR-26a-5p, and miR-338-5p were increased in PsA and regulated synoviocyte activity via PTEN/PI3K/AKT and NFAT5 pathways (40). MiR-26a-5p and miR-130a-3p also demonstrated diagnostic potential and predictive value for therapeutic responsiveness (41).

Synovial and PBMC miRNA networks in PsA

The miR-23a-27a-24-2 cluster displayed tissue-specific patterns: miR-23a was elevated in PBMCs, while all three cluster members were reduced in PsA synovium (14). Synovial miR-23a correlated inversely with disease activity. In vitro silencing experiments revealed that loss of miR-23a enhances synovial fibroblast migration, invasiveness, and production of IL-6, IL-8, MCP-1, regulated upon activation, normal T-cell expressed and secreted (RANTES), and VEGF. Phosphodiesterase 4B (PDE4B) was confirmed as a direct target whose suppression attenuates these inflammatory effects (14).

Regulated miRNAs in PsO without the ability to differentiate PsA

PsO-specific upregulation of miR-155-5p, miR-369-3p, miR-1266-5p, miR-205-5p, and miR-106b-5p was reported (42). These changes did not correlate with PASI, DLQI, disease severity, or nail involvement, likely because the included cohort had a mild-to-moderate phenotype.

Differential biomarkers: miR-941 and miR-210-3p

A study identified miR-941 as significantly elevated in CD14⁺ monocytes from PsA patients but normal in PsO and controls (43). Functionally, miR-941 suppresses WNT16, a key inhibitor of bone resorption (78,79), explaining its alignment with osteoclast-driven joint damage typical of PsA. Similarly, reduced plasma miR-210-3p distinguished PsA from PsO and was proposed as both a diagnostic and therapeutic biomarker (44).

Pharmacogenomic applications of miRNAs in psoriatic disease

Circulating EV miRNAs have shown promise as predictors of methotrexate (MTX) response. MiR-199a-5p, miR-195-5p, miR-196a-5p, and miR-1246 correlated with treatment efficacy, whereas miR-191-5p and miR-21-5p tracked with PsO severity (45). These findings position miRNAs at the intersection of disease activity, drug response, and long-term outcomes.

The central role of the miR-146 family across psoriatic conditions

miR-146a/b in inflammation, genetics, and joint

MiR-146a/b regulates metabolism, differentiation, and immune pathways by repressing nuclear factor kappa B (NF-κB) signaling components (80). MiR-146a is strongly induced by Toll-like receptors (TLRs), IL-1β, and TNF-α (81) and suppresses IRAK1 and TRAF6 in keratinocytes (82). Elevated serum miR-146a-5p was reported in PsA (41), although expression was similar between PsA and RA in another study (38).

Genetic influences

Variants affecting miR-146a biogenesis have been implicated in psoriatic disease. The rs2910164 (G/C) polymorphism was initially reported as more frequent in PsA than in healthy controls (46); however, this association did not always persist in combined analyses, likely reflecting ethnic-specific effects and limited sample sizes, both of which constrain statistical power. Larger studies provided more robust evidence. An Italian cohort of 1,417 individuals identified associations of rs12488457 (COL6A5), rs13081855 (COL8A1), and rs2910164 (miR-146a) with both PsO and PsA, whereas rs3812111 (COL10A1) was uniquely linked to PsA (47). While COL6A5 and COL8A1 participate in inflammatory, proliferative, and angiogenic pathways common to both diseases, COL10A1 is highly enriched in hypertrophic chondrocytes and bone matrix, aligning with the pathological bone remodeling characteristic of PsA, including entheseal involvement and erosive remodeling.

Beyond psoriatic disease, rs2910164 influences susceptibility to various autoimmune conditions (83-85) and is associated with RA in Egyptian populations (86) and with PsO in Chinese cohorts (87). Functionally, the C allele reduces mature miR-146a production, increasing expression of proinflammatory targets and promoting keratinocyte hyperproliferation (87). These findings underscore the context-dependent impact of this SNP on inflammatory signaling.

The IRAK1 rs3027898 polymorphism was identified as the variant most strongly associated with PsA in peripheral blood lymphocytes (48). It was also linked to RA in subsequent analyses (48) and in Chinese cohorts (88). Because IRAK1 is a central kinase within the TLR/IL-1R signaling axis, facilitating MyD88-dependent activation of NF-κB and the downstream production of proinflammatory cytokines (89), genetic perturbations in this pathway may amplify both innate immune responses and chronic inflammation. Given that miR-146a directly suppresses IRAK1 in keratinocytes (82), the interplay between miR-146a genetic variants and IRAK1 polymorphisms likely shapes the inflammatory threshold underlying psoriatic pathology.

The combined expression of miR-146a and IRAK1 was also assessed in lesional skin and PBMCs from patients with cutaneous PsO (49). MiR-146a levels were positively correlated across tissues, indicating coordinated regulation, but no significant differences emerged between “stable” and “progressive” clinical phases, suggesting that miR-146a expression may not reflect short-term disease dynamics. IRAK1 expression, by contrast, was significantly higher in skin lesions than in PBMCs, reinforcing the concept of tissue-specific immune amplification in psoriatic skin. Collectively, these findings support the pathological relevance of the miR-146a/IRAK1 axis across both cutaneous and musculoskeletal compartments.

MiR-146a in osteoclastogenesis and bone remodeling

Beyond its role in innate immune regulation, miR-146a-5p has emerged as a contributor to PsA-specific bone remodeling. Overexpression of miR-146a-5p in CD14⁺ monocytes from PsA patients enhanced osteoclast formation and bone resorption when cells were stimulated with RANKL and TNF-α (50). In vitro blockade of miR-146a-5p markedly reduced osteoclast differentiation and activity, demonstrating a causal relationship between this miRNA and osteoclastogenic drive. Elevated circulating miR-146a-5p levels also correlated with systemic inflammatory markers, including C-reactive protein, and decreased after successful therapeutic response (50), supporting its potential as a dynamic biomarker of inflammatory bone turnover. These findings integrate well with evidence that serum RANKL increases with skin disease severity (90) and that PsA is characterized by excess RANKL combined with reduced osteoprotegerin, tipping the balance toward pathological bone resorption (91,92). Reduced miR-146a activity, as occurs through rs2910164 or downstream dysregulation, may further disinhibit IRAK1-driven inflammatory pathways, amplifying the cytokine milieu (IL-1, TNF-α, IL-6) that primes osteoclastogenesis. Thus, miR-146a appears to operate at the intersection of innate immune activation and structural joint damage, functioning as a molecular bridge between inflammation and bone pathology in PsA.

MiR-21: context-dependent inflammatory modulation in PsO and PsA

MiR-21 is a highly pleiotropic miRNA involved in the regulation of inflammatory signaling, cell differentiation, and tissue remodeling (93,94). Its dysregulation has been documented across chronic inflammatory and autoimmune conditions (95,96), cardiometabolic disease (97,98), and cancer (99), supporting its relevance in psoriatic pathobiology. In early, untreated PsA, miR-21-5p levels were significantly elevated in PBMCs when compared with healthy controls, decreasing after therapy in parallel with improvement in disease activity in psoriatic arthritis (DAPSA) scores (51). Although miR-21-5p did not directly correlate with disease activity at baseline, its reduction following treatment suggests value as a dynamic biomarker of therapeutic response rather than a state marker of inflammation.

Similar findings have been described in PsO, where increased miR-21-5p expression mirrors the pattern observed in PsA, although differences between the two conditions were not statistically significant (51). Significantly, miR-21-5p expression correlates with imaging-detected tenosynovitis (36), a relationship independently confirmed in another study (100), highlighting its potential relevance for entheseal and tendon-associated inflammation. miR-21 upregulation has also been demonstrated in keratinocytes of patients with PsO vulgaris (101), in plaque biopsies (102), and in ankylosing spondylitis, where it is associated with radiographic progression (103). Elevated serum miR-21-5p has been reported in PsA compared with healthy controls (41), and its levels positively correlate with PASI scores in PsO (45), reinforcing its association with cutaneous inflammatory burden. Despite these consistent reports of overexpression, multiple studies have found reduced circulating or cellular miR-21 in PsA, RA, and PsO (38,42), underscoring substantial biological and methodological heterogeneity. This variability is also observed across PsO clinical subtypes. In guttate PsO or anti-TNF-α-induced plaque lesions, miR-21 levels remain low or only mildly elevated, occurring alongside increased tissue inhibitor of metalloproteinase-3 (TIMP-3) (104). Conversely, palmoplantar pustulosis displays heterogeneous miR-21/TIMP-3 patterns (104). These divergent signatures suggest that miR-21 regulation is highly dependent on disease context, phenotype, and possibly local tissue microenvironment, reflecting distinct inflammatory programs across psoriatic variants.

Taken together, miR-21 participates in shared inflammatory pathways across PsO and PsA and shows responsiveness to treatment. However, the high inter-study variability and lack of consistent differential expression between PsO and PsA limit its applicability as a standalone biomarker for distinguishing the two phenotypes. Instead, miR-21 may hold greater value when integrated into multimarker panels or used to monitor therapeutic outcomes in well-characterized clinical cohorts.

Integrative interpretation

Taken together, the available evidence indicates that miR-146a and miR-21 play central roles in amplifying inflammatory programs shared between PsO and PsA, although neither demonstrates consistent discriminatory performance across studies. In contrast, miR-92a-3p, miR-let-7b-5p, miR-30e-5p, miR-941, and miR-210-3p exhibit more substantial potential as PsA-specific biomarkers, particularly when measured in PBMCs or EVs. Additional clusters, such as miR-23a-27a-24-2, and miR-26a-5p and miR-130a-3p, contribute further mechanistic insight, particularly in pathways related to synovial inflammation, bone remodeling, and joint structural damage. These results indicate that reliable differentiation between PsO and PsA will likely depend on combinations of miRNAs, rather than individual markers.

Challenges and limitations for the clinical use of miRNAs

Despite their substantial promise as molecular biomarkers capable of distinguishing PsO from PsA, the translation of miRNAs into clinical practice remains hindered by several methodological and biological challenges. A significant limitation is the lack of standardized protocols across studies. The reviewed literature encompasses heterogeneous biological sample types (serum, plasma, PBMCs, and EVs), diverse analytical platforms (RT-qPCR, microarrays, next-generation sequencing), and inconsistent clinical classification criteria. This variability reduces comparability, complicates replication, and limits meta-analytic integration. Normalization represents an additional challenge. Although several studies employed internal reference miRNAs and hemolysis control assays, no universally accepted normalization strategy for circulating miRNAs has yet been established. Differences in extraction efficiency, hemolysis levels, RNA stabilizers, and the use or absence of exogenous spike-ins continue to influence quantification. As a result, methodological variability persists across studies, introducing noise that may obscure factual biological distinctions between PsO and PsA.

Furthermore, miRNA expression is strongly influenced by extrinsic variables, including age, sex, obesity, smoking, medication exposure, and coexisting inflammatory diseases, creating potential confounders that diminish interpretability when not rigorously controlled. Many available studies suffer from small sample sizes, modest statistical power, and incomplete validation in independent cohorts, restricting the generalizability of reported associations. Analytical models based on isolated miRNAs may oversimplify the complex regulatory networks underlying the transition from cutaneous to articular PsO, further limiting predictive accuracy. Overall, these methodological and biological constraints indicate that while miRNAs have clear mechanistic and diagnostic potential, their clinical deployment will require harmonized methodologies, large-scale longitudinal cohorts, and integrative analytic frameworks capable of capturing complex molecular signatures.

Perspectives and future directions

Current evidence highlights promising circulating and cellular miRNAs with the potential to differentiate PsO from PsA. However, methodological heterogeneity, extraction protocols, normalization strategies, and analytical platforms continue to limit comparisons between studies and restrict translational applicability. Future studies should prioritize methodological standardization, including consensus guidelines for sample processing, reference controls, and reporting practices. Large multicenter cohorts with rigorous phenotypic classification of PsO and PsA, including radiographic, ultrasonographic, and molecular characterization, are essential for validating candidate biomarkers and assessing their predictive value for progression from cutaneous PsO to PsA. Finally, although the present study is a narrative synthesis, the field would benefit from a formal systematic review focused on the most recurrent candidate miRNAs (e.g., miR-146a-5p, miR-21-5p, miR-92a-3p, miR-let-7b-5p, and EV-derived miRNAs). Such an effort would consolidate the evidence, quantify discriminatory performance, and support the development of miRNA-based diagnostic or prognostic panels with clinical applicability.

Conclusions

The reviewed studies converge on a diverse group of miRNAs linked to inflammation, bone remodeling, immune activation, and cellular differentiation, gradually revealing their promise as molecular biomarkers for diagnosis, prognosis, and therapeutic monitoring in psoriatic disease. Among the most recurrent miRNAs were miR-146a-5p, miR-21-5p, miR-92a-3p, miR-126-3p, miR-let-7b-5p, and miR-140. miR-146a-5p showed the strongest mechanistic relevance, participating in TLR/NF-κB regulation, innate immune activation, and osteoclastogenesis, processes essential for PsA pathogenesis. miR-21-5p, frequently elevated across inflammatory contexts, demonstrated potential as a marker of disease severity and therapeutic response. Other miRNAs, including miR-92a-3p, miR-30e-5p, miR-941, and miR-210-3p, exhibited disease-specific patterns that warrant further investigation as differential biomarkers. Despite these promising findings, substantial discrepancies persist across studies, mainly due to methodological variability, differences in population characteristics, sample source, and detection platforms. Standardization of analytical procedures remains a critical barrier to reproducibility and clinical adoption. Furthermore, although several miRNAs have well-defined molecular targets, their biological effects remain difficult to interpret because each miRNA can regulate multiple pathways in a context-dependent manner. In summary, miRNAs represent compelling biomarker candidates for diagnosis, prognosis, and therapeutic monitoring in psoriatic disease. Nonetheless, their clinical applicability depends on overcoming current methodological limitations and conducting extensive, well-designed validation studies to define reliable, clinically meaningful miRNA signatures.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://jlpm.amegroups.com/article/view/10.21037/jlpm-25-38/rc

Peer Review File: Available at https://jlpm.amegroups.com/article/view/10.21037/jlpm-25-38/prf

Funding: This work was supported by the National Council for Scientific and Technological Development (CNPq, Brazil: 313379/2021-1 for R.N.M., 175402/2023-0 for A.P.R.).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jlpm.amegroups.com/article/view/10.21037/jlpm-25-38/coif). R.N.M. serves as an unpaid editorial board member of Journal of Laboratory and Precision Medicine from August 2024 to July 2026. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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