The role of SIRT3-mediated mitochondrial homeostasis in osteoarthritis
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Cellular and Molecular Life Sciences
REVIEW
The role of SIRT3‑mediated mitochondrial homeostasis in osteoarthritis Yuzhe He1 · Zhipeng Wu1 · Langhai Xu1 · Kai Xu1 · Zhonggai Chen1 · Jisheng Ran1 · Lidong Wu1 Received: 4 September 2019 / Revised: 7 February 2020 / Accepted: 2 March 2020 © Springer Nature Switzerland AG 2020
Abstract Osteoarthritis is the most common degenerative joint disease and causes major pain and disability in adults. It has been reported that mitochondrial dysfunction in chondrocytes is associated with osteoarthritis. Sirtuins are a family of nicotinamide adenine dinucleotide-dependent histone deacetylases that have the ability to deacetylate protein targets and play an important role in the regulation of cell physiological and pathological processes. Among sirtuin family members, sirtuin 3, which is mainly located in mitochondria, can exert its deacetylation activity to regulate mitochondrial function, regeneration, and dynamics; these processes are presently recognized to maintain redox homeostasis to prevent oxidative stress in cell metabolism. In this review, we provide present opinions on the effect of mitochondrial dysfunction in osteoarthritis. Furthermore, the potential protective mechanism of SIRT3-mediated mitochondrial homeostasis in the progression of osteoarthritis is discussed. Keywords SIRT3 · Mitochondrion · Oxidative stress · Osteoarthritis
Introduction Osteoarthritis (OA) is a kind of degenerative joint disease mainly associated with clinical manifestations of joint pain and swelling, limited mobility, stiffness, and joint deformities. With its increasing prevalence due to the aging of the population, OA has become a growing health problem that affects 10–15% of all adults over the age of 60 years, with prevalence higher among women than men [1]. At present, there is no effective treatment for osteoarthritis, and the aetiology of this disease includes age, trauma, obesity, strain, joint congenital anomalies, and other factors. Chondrocyte senescence and apoptosis, extracellular matrix degradation with synovial inflammation, and dysfunction of the subchondral bone are the core pathological changes in osteoarthritis [2–4].
* Jisheng Ran [email protected] * Lidong Wu [email protected] 1
Mitochondria, which are defined as the cellular power factories, play roles in some other essential cellular functions, including cell growth, cycle, death, and differentiation. It is increasingly being realized that mitochondria are involved in the progression of osteoarthritis, which is correlated with oxidative stress and reactive oxygen species (ROS) [5, 6]. Furthermore, mitochondrial dysfunction and metabolic impairment have been identified as hallmarks in the initiation and progression of OA, even though chondrocytes are not enriched in mitochondria [7, 8]. Recent studies have concluded that sirtuin 3 (SIRT3), as a mitochondrial nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase, can regulate characteristic mitochondrial processes such as the deacetylation
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