The mitochondrial biogenesis signaling pathway is a potential therapeutic target for myasthenia gravis via energy metabolism (Review)

xlomafota13 shared this article with you from Inoreader The mitochondrial biogenesis signaling pathway is a potential therapeutic target for myasthenia gravis via energy metabolism (Review) Via Experimental and therapeutic medicine Exp Ther Med. 2021 Jul;22(1):702. doi: 10.3892/etm.2021.10134. Epub 2021 May 2. ABSTRACT Myasthenia gravis (MG) is an autoantibody-mediated autoimmune disease that is characterized by muscle weakness and fatigue. Traditional treatments for MG target the neuromuscular junction (NMJ) or the immune system. However, the efficacy of such treatments is limited, and novel therapeutic options for MG are urgently required. In the current review, a new therapeutic strategy is proposed based on the mitochondrial biogenesis and energy metabolism pathway, as stimulating mitochondrial biogenesis and the energy metabolism might alleviate myasthenia gravis. A number of cellular sensors of the energy metabolism were investigated, including AMP-activated protein kinase (AMPK) and sirtuin 1 (SIRT1). AMPK and SIRT1 are sensors that regulate cellular energy homeostasis and maintain energy metabolism by balancing anabolism and catabolism. Peroxisome prolife rator-activated receptor γ coactivator 1α and its downstream transcription factors nuclear respiratory factors 1, nuclear respiratory factors 2, and transcription factor A are key sensors of mitochondrial biogenesis, which can restore mitochondrial DNA and produce new mitochondria. These processes help to control muscle contraction and relieve the symptoms of MG, including muscle weakness caused by dysfunctional NMJ transmission. Therefore, the present review provides evidence for the therapeutic potential of targeting mitochondrial biogenesis for the treatment of MG. PMID:34007311 | PMC:PMC8120506 | DOI:10.3892/etm.2021.10134 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.