The Role of Mitochondrial Metabolism, AMPK-SIRT Mediated Pathway, LncRNA and MicroRNA in Osteoarthritis.
Hao-Yu LiuChi-Fen ChangCheng-Chang LuShun-Cheng WuBin HuangTsung-Lin ChengSung-Yen LinCheng-Jung HoMon-Juan LeeChung-Da YangYing-Chun WangJhong-You LiPing-Cheng LiuChun-Wang WeiLin KangChung-Hwan ChenPublished in: Biomedicines (2022)
Osteoarthritis (OA) is the most common joint disease characterized by degeneration of articular cartilage and causes severe joint pain, physical disability, and impaired quality of life. Recently, it was found that mitochondria not only act as a powerhouse of cells that provide energy for cellular metabolism, but are also involved in crucial pathways responsible for maintaining chondrocyte physiology. Therefore, a growing amount of evidence emphasizes that impairment of mitochondrial function is associated with OA pathogenesis; however, the exact mechanism is not well known. Moreover, the AMP-activated protein kinase (AMPK)-Sirtuin (SIRT) signaling pathway, long non-coding RNA (lncRNA), and microRNA (miRNA) are important for regulating the physiological and pathological processes of chondrocytes, indicating that these may be targets for OA treatment. In this review, we first focus on the importance of mitochondria metabolic dysregulation related to OA. Then, we show recent evidence on the AMPK-SIRT mediated pathway associated with OA pathogenesis and potential treatment options. Finally, we discuss current research into the effects of lncRNA and miRNA on OA progression or inhibition.
Keyphrases
- long non coding rna
- knee osteoarthritis
- protein kinase
- poor prognosis
- oxidative stress
- induced apoptosis
- signaling pathway
- skeletal muscle
- cell death
- ischemia reperfusion injury
- rheumatoid arthritis
- chronic pain
- physical activity
- long noncoding rna
- pain management
- reactive oxygen species
- neuropathic pain
- endoplasmic reticulum
- endoplasmic reticulum stress
- climate change
- drug induced
- combination therapy