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Space exploration's advancement toward long-duration missions prompts intensified research on physiological effects. Despite adaptive physiological stability in some variables, persistent changes affect genome integrity, immune response, and cognitive function. Our study, utilizing multi-omics data from GeneLab, provides crucial insights investigating muscle atrophy during space mission. Leveraging NASA GeneLab's data resources, we apply systems biology-based analyses, facilitating comprehensive understanding and enabling meta-analysis. Through transcriptomics, we establish a reference profile of biological processes underlying muscle atrophy, crucial for intervention development. We emphasize the often-overlooked role of glycosylation in muscle atrophy. Our research sheds light on fundamental molecular mechanisms, bridging gaps between space research and terrestrial conditions. This study underscores the importance of interdisciplinary collaboration and data-sharing initiatives like GeneLab in advancing space medicine research.
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http://dx.doi.org/10.1038/s41526-024-00434-z | DOI Listing |
Lab Anim Res
September 2025
Department of Pathology, Faculty of Medicine, Kindai University, 377-2 Ohno-Higashi, Osaka-Sayama, Osaka, 589-8511, Japan.
Background: Stroke-prone spontaneously hypertensive rats (SHRSP) exhibit slow-twitch muscle-specific hypotrophy compared with normotensive Wistar-Kyoto rats (WKY). Because slow-twitch muscles are prone to disuse atrophy, SHRSP may experience both disuse atrophy and impaired recovery from it. This study investigated the response of SHRSP to disuse atrophy and subsequent recovery, using WKY as a control.
View Article and Find Full Text PDFNature
September 2025
Department of Laboratory Medicine and Pathology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada.
Cancer-associated muscle wasting is associated with poor clinical outcomes, but its underlying biology is largely uncharted in humans. Unbiased analysis of the RNAome (coding and non-coding RNAs) with unsupervised clustering using integrative non-negative matrix factorization provides a means of identifying distinct molecular subtypes and was applied here to muscle of patients with colorectal or pancreatic cancer. Rectus abdominis biopsies from 84 patients were profiled using high-throughput next-generation sequencing.
View Article and Find Full Text PDFMech Ageing Dev
September 2025
Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Rome, Italy; Department of Medicine and Surgery, LUM University, Casamassima, Italy.
Age-related skeletal muscle decline is a major contributor to frailty, functional impairment, and loss of independence in advanced age. This process is characterized by selective atrophy of type II fibers, impaired excitation-contraction coupling, and reduced regenerative capacity. Emerging evidence implicates mitochondrial dysfunction as a central mechanism in the disruption of muscle homeostasis with age.
View Article and Find Full Text PDFArq Gastroenterol
September 2025
Department of GI Surgery, HPB and Liver Transplantation, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
Background: Pancreaticoduodenectomy (PD) is a complex procedure with significant postoperative morbidity. Associated sarcopenia could be a potential risk for increased post-operative complications.
Methods: Patients who had undergone pancreaticoduodenectomy bet-ween July 2019 to December 2020 were included in the study.
Am J Physiol Cell Physiol
September 2025
Department of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC.
Cachexia, the loss of skeletal muscle mass and function with cancer, contributes to reduced life quality and worsened survival. Skeletal muscle fibrosis leads to disproportionate muscle weakness; however, the role of infiltrating immune cells and fibro-adipogenic progenitors (FAPs) in cancer-induced muscle fibrosis is not well understood. Using the C26 model of cancer cachexia, we sought to examine the changes to skeletal muscle immune cells and FAPs which contribute to excessive extracellular matrix (ECM) collagen deposition.
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