Aging Cell最新文献

{"title":"Morphological phenotyping of the aging cochlea in inbred C57BL/6N and outbred CD1 mouse strains.","authors":"Chiara Attanasio, Antonio Palladino, Daniela Giaquinto, Ferdinando Scavizzi, Marcello Raspa, Chiara Peres, Camilla Anastasio, Paola Scocco, Carla Lucini, Paolo de Girolamo, Livia D'Angelo, Elena De Felice","doi":"10.1111/acel.14362","DOIUrl":"https://doi.org/10.1111/acel.14362","url":null,"abstract":"<p><p>Morphological mouse phenotyping plays a pivotal role in the translational setting and even more in the area of auditory research, where mouse is a central model organism due to the evolutionary genetic relationship and morpho-functional analogies with the human auditory system. However, some results obtained in murine models cannot be translated to humans due to the inadequate description of experimental conditions underlying poor reproducibility. We approach the characterization of the aging process of the mouse cochlea in animals up to 18 months of age belonging to two of the most used outbred (CD1) and inbred (C57BL/6N) strains. Striving to reduce any environmental variable we performed our study compliantly to the ARRIVE guidelines. We integrated instrumental data (auditory brainstem response test), with morphological analyses to correlate functional discrepancies to morphological changes and track the differences in the evolution of sensorineural hearing loss in the two strains. We featured the localization of Gipc3, Myosin VIIa, and TMC1 in hair cells of the Corti organ as well as NF 200 and the density of type I neuron in the spiral ganglion. We outlined age-related hearing loss (ARHL) in both strains, and a clear drop in the selected marker localization. However, in CD1 we detected a different trend allowing the identification of potential strain-specific mechanisms, namely an increase in myosin VIIa in 6 months aging mice in comparison to 2 months old animals. Our findings represent an asset to investigate the strain-dependent physiological trigger of ARHL providing new insights in the translational area.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e14362"},"PeriodicalIF":8.0,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142556722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Arginine metabolism is a biomarker of red blood cell and human aging.","authors":"Julie A Reisz, Eric J Earley, Travis Nemkov, Alicia Key, Daniel Stephenson, Gregory R Keele, Monika Dzieciatkowska, Steven L Spitalnik, Eldad A Hod, Steven Kleinman, Nareg H Roubinian, Mark T Gladwin, Kirk C Hansen, Philip J Norris, Michael P Busch, James C Zimring, Gary A Churchill, Grier P Page, Angelo D'Alessandro","doi":"10.1111/acel.14388","DOIUrl":"10.1111/acel.14388","url":null,"abstract":"<p><p>Increasing global life expectancy motivates investigations of molecular mechanisms of aging and age-related diseases. This study examines age-associated changes in red blood cells (RBCs), the most numerous host cell in humans. Four cohorts, including healthy individuals and patients with sickle cell disease, were analyzed to define age-dependent changes in RBC metabolism. Over 15,700 specimens from 13,757 humans were examined, a major expansion over previous studies of RBCs in aging. Multi-omics approaches identified chronological age-related alterations in the arginine pathway with increased arginine utilization in RBCs from older individuals. These changes were consistent across healthy and sickle cell disease cohorts and were influenced by genetic variation, sex, and body mass index. Integrating multi-omics data and metabolite quantitative trait loci (mQTL) in humans and 525 diversity outbred mice functionally linked metabolism of arginine during RBC storage to increased vesiculation-a hallmark of RBC aging-and lower post-transfusion hemoglobin increments. Thus, arginine metabolism is a biomarker of RBC and organismal aging, suggesting potential new targets for addressing sequelae of aging.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e14388"},"PeriodicalIF":8.0,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142542256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of cysteine on lifespan in three model organisms: A systematic review and meta-analysis.","authors":"Yue Ma, Mengqi Chen, Kaiyao Huang, Wakam Chang","doi":"10.1111/acel.14392","DOIUrl":"https://doi.org/10.1111/acel.14392","url":null,"abstract":"<p><p>Cysteine is an amino acid present in thiol proteins and often dictates their secondary structures. Although considered nonessential, cysteine may be essential for patients with certain metabolic diseases and can reduce the requirement for dietary methionine. Cysteine and some of its derivatives, such as N-acetylcysteine, are considered antioxidants and widely used in animal aging studies. To provide insights into the potential anti-aging effects of cysteine, we systematically reviewed and performed a meta-analysis to investigate the impact of cysteine supplementation on lifespan using three model organisms: mice, nematodes, and fruit flies. A total of 13 mouse studies, 13 C. elegans studies, and 5 Drosophila studies were included in the analysis. The findings revealed that cysteine supplementation significantly reduced the risk of mortality in mice and C. elegans. Subgroup analysis showed consistent results across different starting times and administration methods and revealed adverse effects of high doses on worms and a lack of effect in nondisease mouse models. Similar to mice, the effects of cysteine supplementation on Drosophila were not statistically significant, except in transgenic flies. The study identified certain limitations, including the quality of the included studies and the potential for publication bias. We also discussed uncertainties in the underlying molecular mechanisms and the clinical application of dietary cysteine.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e14392"},"PeriodicalIF":8.0,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142542259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heat exposure promotes sarcopenia via gut microbiota-derived metabolites.","authors":"Yi-Fan Guo, Zhe-Yu Liu, Min Zhou, Wei-Hong Kuang, Ya Liu, Yan Huang, Ping Yin, Zhu-Ying Xia","doi":"10.1111/acel.14370","DOIUrl":"https://doi.org/10.1111/acel.14370","url":null,"abstract":"<p><p>The unprecedented rise in global ambient temperatures in the last decade has significantly impacted human health, yet how heat exposure affects the development of sarcopenia remains enigmatic. Here, we demonstrate that chronic heat exposure induces skeletal muscle volume loss, leading to muscle strength and functional decline in mice. The microbiota composition of heat-exposed mice was analyzed using 16S ribosomal DNA analysis. Liquid chromatography-mass spectrometry (LC-MS) was used to explore the effects of heat exposure on the blood metabolome and to further analyze the correlation between blood metabolism and gut microbiota. Transplantation of microbiota from heat-exposed mice to germ-free mice was sufficient to increase adverse effects on skeletal muscle function in the host. Mechanistically, using an untargeted metabolomics strategy, we reveal that altered gut microbiota due to high temperatures is associated with elevated serum levels of homocitrulline. Homocitrulline causes mitochondrial dysfunction in myocytes by exacerbating ferroptosis levels. And Nrf2 activator (Oltipraz) supplementation alleviates muscle atrophy and dysfunction induced by heat exposure. Our findings reveal the detrimental effects of heat exposure on muscle function and provide new strategies for treating sarcopenia.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e14370"},"PeriodicalIF":8.0,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142520448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Legumain deficiency halts atherogenesis by modulating T cell receptor signaling.","authors":"Xuying Xiang, Feng Zhang, Lei Nie, Xiaoqing Guo, Mengting Qin, Jiaojiao Chen, Dailiang Jiang, Zhentao Zhang, Ling Mao","doi":"10.1111/acel.14391","DOIUrl":"https://doi.org/10.1111/acel.14391","url":null,"abstract":"<p><p>Atherosclerosis is an age-related pathological process associated with elevated levels of legumain in plaques and plasma. However, the underlying mechanisms remain unclear. The aim of this study was to investigate the role of legumain in the progression of atherosclerotic plaques, with a particular focus on functional and phenotypic changes in CD4⁺ T cells. Apolipoprotein E-deficient (Apoe^-/-) mice were crossed with legumain-deficient (Lgmn^-/-) mice to generate Lgmn^-/-Apoe^-/- mice. CD4⁺ T cells accumulated in the atherosclerotic plaques of Apoe^-/- mice fed a high-fat diet. Deletion of legumain attenuated the deposition of CD4⁺ T cells in plaques and reduced the number of atherosclerotic lesions. The levels of CD4⁺ T cells in the blood, lymph nodes, and spleen were decreased in Lgmn^-/- mice. Transcriptomic analysis revealed that the deletion of legumain decreased the differentiation, survival, and function of CD4⁺ memory T cells by suppressing the T cell receptor (TCR) signaling pathway. These changes are accompanied by the downregulation of the antiapoptotic protein B-cell lymphoma 2 (Bcl-2) and the reduced release of interleukin (IL)-2 and interferon (IFN)-γ. These results suggest that legumain deficiency may play a role in the development of atherosclerosis by impairing the survival, proliferation, and function of CD4⁺ T cells. Inhibition of legumain activity may be an innovative therapy for the treatment of atherosclerosis.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e14391"},"PeriodicalIF":8.0,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142542258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aging alters the effect of adiponectin receptor signaling on bone marrow-derived mesenchymal stem cells.","authors":"Hanghang Liu, Qiucheng Zhao, Shibo Liu, Bolun Li, Zizhuo Zheng, Yao Liu, Pei Hu, En Luo","doi":"10.1111/acel.14390","DOIUrl":"https://doi.org/10.1111/acel.14390","url":null,"abstract":"<p><p>Adiponectin receptor signaling represents a promising therapeutic target for age-related conditions such as osteoporosis and diabetes. However, the literature presents conflicting evidence regarding the role of adiponectin signaling in bone homeostasis and fracture repair across different health states, ages, and disease conditions. These inconsistencies may arise from the complex endocrine and paracrine feedback mechanisms regulating adiponectin, as well as the variability in adiponectin isoforms and receptor expressions. In this study, we observed differential expression of adiponectin receptors in the bone marrow (BM) of aged mice, characterized by elevated levels of adiponectin receptor 2 and reduced levels of receptor 1, as corroborated by both single-cell sequencing and in vivo staining. Additionally, circulating levels of adiponectin and its local expression were significantly higher in aged mice compared to younger counterparts. Treatment with adiponectin receptor agonist, AdipoRon, enhanced bone regeneration and repair in young mice by promoting osteogenesis and reducing osteoclastogenesis. Conversely, in aged mice, AdipoRon treatment led to cellular senescence, delayed bone repair, and inhibited osteogenic activity. Notably, the adiponectin receptor 1-Wnt and adiponectin receptor 2-MAPK and mTOR signaling pathways were differentially activated in AdipoRon-treated BM mesenchymal stem cells from young and aged mice. Additionally, the NF-κB, and AKT pathways were consistently downregulated in BM macrophages of both age groups following AdipoRon administration. In conclusion, aging significantly modulates the impact of adiponectin receptor signaling on BM mesenchymal stem cells. This modulation is potentially attributable to changes in receptor transcription and distribution, as well as differential activation of downstream signaling pathways.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e14390"},"PeriodicalIF":8.0,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142491452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic polypharmacy, monotherapy, and deprescribing: Understanding complex effects on the hepatic proteome of aging mice.","authors":"Kevin Winardi, John Mach, Matthew J McKay, Mark P Molloy, Sarah J Mitchell, Michael R MacArthur, Catriona McKenzie, David G Le Couteur, Sarah N Hilmer","doi":"10.1111/acel.14357","DOIUrl":"https://doi.org/10.1111/acel.14357","url":null,"abstract":"<p><p>Polypharmacy (use of ≥5 concurrent medications) is highly prevalent among older adults to manage chronic diseases and is linked to adverse geriatric outcomes, including physical and cognitive functional impairments, falls, frailty, hospitalization, and mortality. Deprescribing (withdrawal) is a potential strategy to manage polypharmacy. The broad molecular changes by which polypharmacy causes harm and deprescribing may be beneficial are unknown and unfeasible to study rigorously in tissue from geriatric patients. Therefore, in a randomized controlled trial, we administered therapeutic doses of commonly used chronic medications (oxycodone, oxybutynin, citalopram, simvastatin, or metoprolol) as monotherapy or concurrently (polypharmacy) from middle-age (12 months) to old-age (26 months) to male C57BL/6J (B6) mice and deprescribed (gradually withdrew) treatments in a subset from age 21 months. We compared drug-related hepatic effects by applying proteomics along with transcriptomics and histology. We found that monotherapy effects on hepatic proteomics were limited but significant changes were seen with polypharmacy (93% unique to polypharmacy). Polypharmacy altered the hepatic expression of proteins involved in immunity, and in drug, cholesterol, and amino acid metabolism, accompanied by higher serum drug levels than monotherapies. Deprescribing not only reversed some effects but also caused irreversible and novel changes in the hepatic proteome. Furthermore, our study identified several hepatic protein co-expressed modules that are associated with clinically relevant adverse geriatric outcomes, such as mobility, frailty, and activities of daily living. This study highlights the complex molecular changes following aging, chronic polypharmacy, and deprescribing. Further exploration of these mechanistic pathways may inform management of polypharmacy and deprescribing in older adults.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e14357"},"PeriodicalIF":8.0,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142491454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuronal cathepsin S increases neuroinflammation and causes cognitive decline via CX3CL1-CX3CR1 axis and JAK2-STAT3 pathway in aging and Alzheimer's disease.","authors":"Pei-Pei Liu, Xiao-Hui Liu, Ming-Jing Ren, Xiao-Tong Liu, Xiao-Qing Shi, Ming-Li Li, Shu-Ang Li, Yang Yang, Dian-Dian Wang, Yue Wu, Fan-Xiang Yin, Yan-Hong Guo, Run-Zhou Yang, Meng Cheng, Yong-Juan Xin, Jian-Sheng Kang, Bing Huang, Kai-Di Ren","doi":"10.1111/acel.14393","DOIUrl":"https://doi.org/10.1111/acel.14393","url":null,"abstract":"<p><p>Aging is an intricate process involving interactions among multiple factors, which is one of the main risks for chronic diseases, including Alzheimer's disease (AD). As a member of cysteine protease, cathepsin S (CTSS) has been implicated in inflammation across various diseases. Here, we investigated the role of neuronal CTSS in aging and AD started by examining CTSS expression in hippocampus neurons of aging mice and identified a significant increase, which was negatively correlated with recognition abilities. Concurrently, we observed an elevation of CTSS concentration in the serum of elderly people. Transcriptome and fluorescence-activated cell sorting (FACS) results revealed that CTSS overexpression in neurons aggravated brain inflammatory milieu with microglia activation to M1 pro-inflammatory phenotype, activation of chemokine C-X3-C-motif ligand 1 (CX3CL1)-chemokine C-X3-C-motif receptor 1 (CX3CR1) axis and janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 (STAT3) pathway. As CX3CL1 is secreted by neurons and acts on the CX3CR1 in microglia, our results revealed for the first time the role of neuron CTSS in neuron-microglia \"crosstalk.\" Besides, we observed elevated CTSS expression in multiple brain regions of AD patients, including the hippocampus. Utilizing CTSS selective inhibitor, LY3000328, rescued AD-related pathological features in APP/PS1 mice. We further noticed that neuronal CTSS overexpression increased cathepsin B (CTSB) activity, but decreased cathepsin L (CTSL) activity in microglia. Overall, we provide evidence that CTSS can be used as an aging biomarker and plays regulatory roles through modulating neuroinflammation and recognition in aging and AD process.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e14393"},"PeriodicalIF":8.0,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142491456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early resilience and epigenetic ageing: Results from the prospective Young Finns Study with a 31-year follow-up.","authors":"Saarinen Aino, Marttila Saara, P Mishra Pashupati, Lyytikäinen Leo-Pekka, Hamal Mishra Binisha, Raitoharju Emma, Mononen Nina, Kähönen Mika, Raitakari Olli, Lehtimäki Terho, Keltikangas-Järvinen Liisa","doi":"10.1111/acel.14394","DOIUrl":"https://doi.org/10.1111/acel.14394","url":null,"abstract":"<p><p>Evidence is accumulating on the connection of early adversities and harsh family environment with epigenetic ageing. We investigated whether early psychosocial resilience is associated with epigenetic ageing in adulthood. We used the population-based Young Finns data (n = 1593). Early psychosocial resilience was assessed in 1980-1989 across five broad domains: (1) index of psychological strength (self-esteem at home/in general/at school, perceived possibilities to influence at home, internal life control), (2) index of social satisfaction (perceived support from family/friends and life satisfaction), (3) index of leisure time activities (hobbies and physical fitness), (4) index of responsible health behaviors (infrequent smoking or alcohol consumption), and (5) index of school career (school grades and adaptation). Epigenetic ages were calculated for blood samples from 2011, and the analyses were performed with variables describing age deviation (AgeDev_Hannum, AgeDev_Horvath, AgeDev_Pheno, AgeDev_Grim) and DunedinPACE. Covariates included early family environment, polygenic risk scores for schizophrenia and major depression, adulthood education, and adulthood health behaviors. All of the early resilience indexes were associated with lower levels of epigenetic ageing in adulthood, most consistently with AgeDev_Grim and DunedinPACE. The associations of psychological strength and social satisfaction, in particular, seemed to be non-linear. In a smaller subsample (n = 289), high early resilience was related to lower AgeDev_Grim over a 25-year follow-up in those who had high \"baseline\" levels of AgeDev_Grim. In conclusion, early resilience seems to associate with lower level of epigenetic ageing in adulthood. Our results tentatively suggest that early resilience may increase \"equality in epigenetic ageing\" in a general population.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e14394"},"PeriodicalIF":8.0,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142491455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Time-restricted feeding mediated modulation of microbiota leads to changes in muscle physiology in Drosophila obesity models.","authors":"Christopher Livelo, Yiming Guo, Jagathnarayan Madhanagopal, Casey Morrow, Girish C Melkani","doi":"10.1111/acel.14382","DOIUrl":"https://doi.org/10.1111/acel.14382","url":null,"abstract":"<p><p>Recent research has highlighted the essential role of the microbiome in maintaining skeletal muscle physiology. The microbiota influences muscle health by regulating lipid metabolism, protein synthesis, and insulin sensitivity. However, metabolic disturbances such as obesity can lead to dysbiosis, impairing muscle function. Time-restricted feeding (TRF) has been shown to mitigate obesity-related muscle dysfunction, but its effects on restoring healthy microbiomes remain poorly understood. This study utilizes 16S microbiome analysis and bacterial supplementation to investigate the bacterial communities influenced by TRF that may benefit skeletal muscle physiology. In wild-type and obese Drosophila models (axenic models devoid of natural microbial communities), the absence of microbiota influence muscle performance and metabolism differently. Specifically, axenic wild-type Drosophila exhibited reduced muscle performance, higher glucose levels, insulin resistance, ectopic lipid accumulation, and decreased ATP levels. Interestingly, in obese Drosophila (induced by a high-fat diet or predisposed obesity mutant Sk2), the absence of microbiota improved muscle performance, lowered glucose levels, reduced insulin resistance, and increased ATP levels. TRF was found to modulate microbiota composition, notably increasing Acetobacter pasteurianus (AP) and decreasing Staphylococcus aureus (SA) in both obesity models. Supplementation with AP improved muscle performance and reduced glucose and insulin resistance, while SA supplementation had the opposite effect. This study provides novel insights into the complex interactions between TRF, microbiota, and skeletal muscle physiology in different Drosophila models.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e14382"},"PeriodicalIF":8.0,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142491458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}