Abstract
Osteoarthritis (OA) is a prevalent and debilitating age-related joint disease characterized by articular cartilage degeneration, synovial membrane inflammation, osteophyte formation, as well as subchondral bone sclerosis. OA drugs at present are mainly palliative and do not halt or reverse disease progression. Currently, no disease-modifying OA drugs (DMOADs) are available and total joint arthroplasty remains a last resort. Therefore, there is an urgent need for the development of efficacious treatments for OA management. Among all novel pharmaco-therapeutical options, exosome-based therapeutic strategies are highly promising. Exosome cargoes, which include proteins, lipids, cytokines, and various RNA subtypes, are potentially capable of regulating intercellular communications and gene expression in target cells and tissues involved in OA development. With extensive research in recent years, exosomes in OA studies are no longer limited to classic, mesenchymal stem cell (MSC)-derived vesicles. New origins, structures, and functions of exosomes are constantly being discovered and investigated. This review systematically summarizes the non-classic origins, biosynthesis, and extraction of exosomes, describes modification and delivery techniques, explores their role in OA pathogenesis and progression, and discusses their therapeutic potential and hurdles to overcome in OA treatment.
Highlights
Exosomes from healthy chondrocytes had high bioactivity in the elimination of mitochondrial dysfunction and restoration of immune reaction by regulating M2 macrophage penetration, delaying OA progression [31]. These chondrocyte-derived exosomes contained miR-8485, which inhibited the expression of glycogen synthase kinase (GSK)-3β and activated the Wnt/β-catenin pathway, promoting the chondrogenic differentiation of bone marrow MSC (BMSC) [69]
Wu et al found that exosomes produced by osteoblasts in osteoarthritic, sclerotic subchondral bone contained a high level of miR-210-5p, which decreased the rate of oxygen consumption by chondrocytes, altered their bioenergetic state, and accelerated the progression of cartilage degeneration [32]
Previous studies showed that exosomes originating from platelets were sufficient to enhance anabolic marker expression and prevent the release of proinflammatory cytokines in chondrocytes derived from OA patients, showing the same regulatory effects as the full blood product [51]
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. No disease-modifying osteoarthritis drugs (DMOADs) are available to reverse or halt OA progression [8] Pharmacological approaches, such as the use of Bioengineering 2022, 9, 99. Pharmacological approaches, such as the use of nonsteroidal anti-inflammatory drugs (NSAIDs), drugs analgesics, and surgical interventions areinterventions non-steroidal anti-inflammatory (NSAIDs), analgesics, and surgical current options to offer symptomatic relief [9]. We discuss the biosynthesis, origins, and contents of exoexosomes, and review their roles in OA pathogenesis, progression, and treatment.
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