Oxidative Stress, MicroRNAs, and Long Non-Coding RNAs in Osteoarthritis Pathogenesis: Cross-Talk and Molecular...

Area of Science:

• Biochemistry
• Molecular Biology
• Genetics

Background:

• Osteoarthritis (OA) is a prevalent degenerative joint disease marked by cartilage degradation, inflammation, and lesions.
• Non-coding RNAs (ncRNAs) are critical regulators of gene expression, including cartilage homeostasis, and their dysregulation contributes to OA.
• Oxidative stress exacerbates OA pathogenesis by promoting inflammation, extracellular matrix degradation, and chondrocyte apoptosis.

Purpose of the Study:

• To review the intricate roles of oxidative stress, microRNAs (miRNAs), and long non-coding RNAs (lncRNAs) in osteoarthritis (OA).
• To elucidate the molecular mechanisms underlying the cross-talk between oxidative stress and ncRNAs in OA pathogenesis.
• To identify potential diagnostic and therapeutic targets for OA based on these molecular interactions.

Main Methods:

• Literature review of studies investigating ncRNAs, oxidative stress, and OA.
• Analysis of the interplay between oxidative stress and altered expression of miRNAs and lncRNAs in OA.
• Synthesis of current knowledge on molecular mechanisms and potential therapeutic strategies.

Main Results:

• ncRNAs, particularly miRNAs and lncRNAs, are deregulated in OA, impacting genes involved in cartilage degradation and inflammation.
• A reciprocal relationship exists between altered ncRNA expression and oxidative stress in OA.
• These molecular players contribute to chondrocyte apoptosis, extracellular matrix breakdown, and inflammatory responses in OA.

Conclusions:

• Oxidative stress and deregulated ncRNAs (miRNAs, lncRNAs) are key contributors to OA pathogenesis.
• Understanding the cross-talk between these factors is crucial for developing novel OA diagnostics and therapeutics.
• Targeting these pathways may offer new avenues for managing osteoarthritis.