Intertwined roles of microRNA-155 and metformin in osteoarthritis: Novel potential diagnostic, prognostic, and therapeutic modulators

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Osteoarthritis (OA) is a chronic joint disease characterized by cartilage degradation, synovial inflammation, and subchondral bone remodelling. Despite its increasing prevalence, effective diagnostic, disease-limiting, and therapeutic strategies remain unattainable. Recent studies have recognized the involvement of microRNA-155 (miR-155) in the pathogenesis of OA and most of its risk factors while also identifying the antidiabetic drug metformin as a potential modulator of disease progression. MiR-155, a key endogenous regulator of the immune system, mechano-transduction, and multiple genetic pathways, interacts with OA targets of cellular energetic and circadian homeostasis, promoting systemic and local articular inflammation, cartilage matrix degradation, and chondrocyte apoptosis. Metformin, widely used for type 2 diabetes, has demonstrated anti-inflammatory, anti-oxidative, and chondroprotective properties in OA, mainly through its activation of adenosine monophosphate-activated protein kinase and inhibition of nuclear factor kappa-B signalling. Enthrallingly, metformin targets the same cellular pathways as miR-155 with emerging evidence also suggesting miR-155 expression modulation, indicating synergistic, potentially disease-modifying effects in OA. This review highlights the central role of miR-155 in OA pathophysiology and its potential as a biomarker for disease diagno

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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