On the basis of the accelerated age-related effects in type II muscle, we hypothesized that with aging the semimembranosus (type II) muscle would accumulate a greater amount of oxidized proteins compared to proteins in the soleus (type I) muscle. In this study, 3-nitrotyrosine (3-NT) was used as a stable marker of protein oxidative damage. The presence of 3-NT was evaluated in muscles from young adult, old, and very old Fischer 344 rats to provide an indication of the time course of muscle protein oxidative damage. A significant age-associated increase in nitrotyrosine-modified proteins was observed. The modified proteins identified by matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry include the sarcoplasmic reticulum Ca(+2)-ATPase, aconitase, beta-enolase, triosephosphate isomerase, and carbonic anhydrase III. These proteins, involved in metabolism and calcium homeostasis, exhibited an age-dependent increase in 3-NT content in both muscles. However, significant levels of 3-NT modification were present at an earlier age in the semimembranosus muscle.
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http://dx.doi.org/10.1093/gerona/61.8.806 | DOI Listing |
Sleep Breath
January 2025
Department of Pulmonary and Critical Care Medicine, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, No.1 Da Hua Road, Dong Dan, Dongcheng District, Beijing, 100730, PR China.
Purpose: To investigate the relationship between obstructive sleep apnea hypopnea syndrome (OSAHS) severity and fat, bone, and muscle indices.
Methods: This study included 102 patients with OSAHS and retrospectively reviewed their physical examination data. All patients underwent polysomnography, body composition analysis, dual-energy X-ray absorptiometry, computed tomography (CT) and blood test.
Cell Mol Life Sci
January 2025
Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, Unitat de Farmacologia, Universitat de Barcelona, Av. Joan XXIII 27-31, 08028, Barcelona, Spain.
Nuclear growth differentiation factor 15 (GDF15) reduces the binding of the mothers' against decapentaplegic homolog (SMAD) complex to its DNA-binding elements. However, the stimuli that control this process are unknown. Here, we examined whether saturated fatty acids (FA), particularly palmitate, regulate nuclear GDF15 levels and the activation of the SMAD3 pathway in human skeletal myotubes and mouse skeletal muscle, where most insulin-stimulated glucose use occurs in the whole organism.
View Article and Find Full Text PDFFASEB J
January 2025
National Key Laboratory of Space Medicine, China Astronaut Research and Training Center, Beijing, China.
Microgravity-induced cardiac remodeling and dysfunction present significant challenges to long-term spaceflight, highlighting the urgent need to elucidate the underlying molecular mechanisms and develop precise countermeasures. Previous studies have outlined the important role of miRNAs in cardiovascular disease progression, with miR-199a-3p playing a crucial role in myocardial injury repair and the maintenance of cardiac function. However, the specific role and expression pattern of miR-199a-3p in microgravity-induced cardiac remodeling remain unclear.
View Article and Find Full Text PDFBiophys J
January 2025
Department of Pharmacology, University of California Davis, California 95616.
In every heartbeat, cardiac muscle cells perform excitation-Ca signaling-contraction (EC) coupling to pump blood against the vascular resistance. Cardiomyocytes can sense the mechanical load and activate mechano-chemo-transduction (MCT) mechanism, which provides feedback regulation of EC coupling. MCT feedback is important for the heart to upregulate contraction in response to increased load to maintain cardiac output.
View Article and Find Full Text PDFCell Commun Signal
January 2025
Department of Vascular & Cardiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Purpose: Cardiomyocyte death is a major cytopathologic response in acute myocardial infarction (AMI) and involves complex inflammatory interactions. Although existing reports indicating that mixed lineage kinase domain-like protein (MLKL) is involved in macrophage necroptosis and inflammasome activation, the downstream mechanism of MLKL in necroptosis remain poorly characterized in AMI.
Methods: MLKL knockout mice (MLKL), RIPK3 knockout mice (RIPK3), and macrophage-specific MLKL conditional knockout mice (MLKL) were established.
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