Exercise is a well-known stimulus for the expansion of the mitochondrial pool within skeletal muscle. Mitochondria have a remarkable ability to remodel their networks and can respond to an array of signaling stimuli following contractile activity to adapt to the metabolic demands of the tissue, synthesizing proteins to expand the mitochondrial reticulum. In addition, when they become dysfunctional, these organelles can be recycled by a specialized intracellular system. The signals regulating this mitochondrial life cycle of synthesis and degradation during exercise are still an area of great research interest. As mitochondrial turnover has valuable consequences in physical performance, in addition to metabolic health, disease, and aging, consideration of the signals which control this cycle is vital. This review focuses on the regulation of mitochondrial turnover in skeletal muscle and summarizes our current understanding of the impact that exercise has in modulating this process.
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http://dx.doi.org/10.1016/bs.pmbts.2015.07.007 | DOI Listing |
Discov Med
December 2024
Department of Respiratory Medicine, The First Affiliated Hospital of Anhui University of Chinese Medicine, 230031 Hefei, Anhui, China.
Background: Chronic obstructive pulmonary disease (COPD) is a prevalent yet manageable respiratory condition. However, treatments presently used normally have side effects and cannot cure COPD, making it urgent to explore effective medications. The ginsenoside Rg3 (Rg3) has been shown to have anti-inflammatory and anti-tumor properties and can improve COPD.
View Article and Find Full Text PDFRespir Res
December 2024
Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
Backgroud: Recent studies have reported mitochondrial damage and metabolic dysregulation in BPD, but the changes in mitochondrial dynamics and glucose metabolic reprogramming in ATII cells and their regulatory relationship have not been reported.
Methods: Neonatal rats in this study were divided into model (FIO2:85%) and control (FIO2: 21%) groups. Lung tissues were extracted at 3, 7, 10 and 14 postnatal days and then conducted HE staining for histopathological observation.
Nan Fang Yi Ke Da Xue Xue Bao
December 2024
Anhui Provincial Center for Neural Regeneration Technology and New Medical Materials Engineering Research, Bengbu Medical University, Bengbu 233000, China.
Objectives: To investigate the role of mitochondrial autophagy disorder caused by deletion of E3 ubiquitin ligase Parkin in neuroinflammation in a mouse model of MPTP-induced Parkinson's disease (PD).
Methods: Wild-type (WT) male C57BL/6 mice and Parkin mice were given intraperitoneal injections with MPTP or PBS for 5 consecutive days, and the changes in motor behaviors of the mice were observed using open field test. The effects of Parkin deletion on PD development and neuroinflammation were evaluated using immunofluorescence and Western blotting.
J Cachexia Sarcopenia Muscle
February 2025
Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA.
Background: Inclusion body myositis (IBM) is the most prevalent muscle disease in adults for which no current treatment exists. The pathogenesis of IBM remains poorly defined. In this study, we aimed to explore the interplay between inflammation and mitochondrial dysfunction in IBM.
View Article and Find Full Text PDFMetabolism
December 2024
Department of Endocrinology and Diabetology, Medical Faculty and University Hospital Düsseldorf, Heinrich-Heine-University, Düsseldorf, Germany; Institute for Clinical Diabetology, German Diabetes Center, Leibniz Institute for Diabetes Research at Heinrich-Heine-University, Düsseldorf, Germany; German Center for Diabetes Research, Partner Düsseldorf, Neuherberg, Germany.
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