Introduction: The mitochondrial network within cells is mediated by fission and fusion processes.
Methods: We investigated the expression of the proteins responsible for these events during conditions of altered oxidative capacity.
Results: With chronic contractile activity, the mitochondrial reticulum increased in size, along with concomitant increases in the fusion proteins Opa1 and Mfn2 (by 36% and 53%; P < 0.05). When we induced muscle disuse through denervation for 7 days, fragmented mitochondria were observed, along with significant decreases in the expression of Mfn2 and Opa1 (by 84% and 70%). To assess the effects of aging on mitochondrial morphology, young (5 month) and aged (35 month) Fisher 344 Brown Norway rats were used. Aged animals also possessed smaller mitochondria and displayed increased levels of fission proteins.
Conclusions: Chronic muscle use increases the ratio of fusion:fission proteins, leading to reticular mitochondria, whereas muscle disuse and aging result in a decrease in this ratio, culminating in fragmented organelles.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1002/mus.23838 | DOI Listing |
Environ Toxicol
January 2025
Cardiovascular Center, College of Medicine, University of Cincinnati, Cincinnati, Ohio, USA.
The cardiovascular risks linked to PM include calcification in both vasculature and myocardial tissues, leading to structural changes and functional decline. Through the selection of a clinically proven endogenous agent, sodium thiosulfate (STS), capable of addressing PM related cardiac abnormalities, we not only address the absence of effective solutions to mitigate PM toxicity, but also provide evidence for the repurposing potential of STS in ameliorating PM induced cardiac damage. Female Wistar rats were exposed to PM (250 μg/m) for 3 h daily for 21 days.
View Article and Find Full Text PDFJ Headache Pain
January 2025
Department of Hand and Foot Surgery, China-Japan Union Hospital of Jilin University, Changchun, China.
Neuropathic pain poses a significant clinical challenge, largely due to the incomplete understanding of its molecular mechanisms, particularly the role of mitochondrial dysfunction. Bioinformatics analysis revealed that pyroptosis and inflammatory responses induced by spared nerve injury (SNI) in the spinal dorsal horn play a critical role in the initiation and persistence of neuropathic pain. Among the factors involved, TSPO (translocator protein) emerged as a key regulator.
View Article and Find Full Text PDFIn Vitro Cell Dev Biol Anim
January 2025
Department of Outpatient Service, The Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, Hengyang, 421002, Hunan, China.
The objective of this study is to explore how adipose-derived stem cells (ASCs) regulate mitochondrial structure and function and the impact of this regulation on slowing cellular senescence. HFF-1 cells were induced by HO to establish a cellular senescence model, and ASCs or Mdivi-1 (mitochondrial fission inhibitor) was added. MTT examined the cell proliferation; flow cytometry detected mitochondrial membrane potential as well as apoptosis and cell cycle; kit measured ATP production; ELISA analyzed the levels of interleukin-6 (IL-6), interleukin 1 beta (IL-1β), tumor necrosis factor alpha-like (TNF-α), glutathione (GSH), malondialdehyde (MDA), and superoxide dismutase (SOD); Western blotting and qRT-PCR detected the expression of protein and mRNA levels; and β-galactosidase staining observed the degree of cellular senescence.
View Article and Find Full Text PDFMol Plant Microbe Interact
January 2025
USDA ARS, Horticultural Crops Research Laboratory, 3420 NW Orchard Ave., Corvallis, Oregon, United States, 97330;
Members of the genus are responsible for many important diseases in agricultural and natural ecosystems. causes devastating diseases of oak, and tanoak stands in US forests and larch in the UK. The four evolutionary lineages involved express different virulence phenotypes on plant hosts, and characterization of gene content is foundational to understanding the basis for these differences.
View Article and Find Full Text PDFHeliyon
January 2025
School of Chemical and Biotechnology, SASTRA Deemed University, Tirumalaisamudram, Thanjavur, Tamil Nadu, India.
Background: Growing evidence indicates that disruptions in mitochondrial quality management contribute to the development of acute kidney injury (AKI), incomplete or maladaptive kidney repair, and chronic kidney disease. However, the temporal dynamics of mitochondrial quality control alterations in relation to renal injury and its recovery remain poorly understood and are addressed in this manuscript.
Method: ology: Male Wistar rats (n = 60) were subjected to varying durations of ischemia and reperfusion.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!