Article
Cardiac & Cardiovascular Systems
Junichi Matsumoto, Shingo Takada, Takaaki Furihata, Hideo Nambu, Naoya Kakutani, Satoshi Maekawa, Wataru Mizushima, Ippei Nakano, Arata Fukushima, Takashi Yokota, Shinya Tanaka, Haruka Handa, Hisataka Sabe, Shintaro Kinugawa
Summary: The study showed that treatment with rhBDNF improved exercise capacity in mice with heart failure through enhancing fatty acid oxidation via the activation of the AMPK alpha-PGC1 alpha axis in skeletal muscle. This suggests that BDNF may be a potential therapeutic option to improve exercise capacity in heart failure.
CIRCULATION-HEART FAILURE
(2021)
Article
Cardiac & Cardiovascular Systems
Jeanne du Fay de Lavallaz, Alexandra Prepoudis, Maria Janina Wendebourg, Eva Kesenheimer, Diego Kyburz, Thomas Daikeler, Philip Haaf, Julia Wanschitz, Wolfgang N. Loescher, Bettina Schreiner, Mira Katan, Hans H. Jung, Britta Maurer, Angelika Hammerer-Lercher, Agnes Mayr, Danielle M. Gualandro, Annemarie Acket, Christian Puelacher, Jasper Boeddinghaus, Thomas Nestelberger, Pedro Lopez-Ayala, Noemi Glarner, Samyut Shrestha, Robert Manka, Joanna Gawinecka, Salvatore Piscuoglio, John Gallon, Sophia Wiedemann, Michael Sinnreich, Christian Mueller
Summary: This study aimed to confirm the cardiac specificity of cTnT in patients with various skeletal muscle disorders (SMDs). The results showed that elevations in cTnT concentrations in patients with active chronic SMDs are common and not attributable to cardiac disease, while this phenomenon was not observed for cTnI. The re-expression of cTnT in skeletal muscle may partially explain this.
Article
Biochemistry & Molecular Biology
Wujing Ren, Zujie Xu, Shou Pan, Yixuan Ma, Hangzhuo Li, Fangnan Wu, Wenyan Bo, Mengxin Cai, Zhenjun Tian
Summary: Skeletal muscle in patients with heart failure undergoes changes in structure, function, and metabolism. Oxidative stress and cell apoptosis play a role in the development of skeletal muscle atrophy induced by myocardial infarction (MI) and heart failure (HF). Aerobic exercise (AE) has been shown to prevent skeletal muscle atrophy after MI, but the underlying mechanism and molecular targets are not fully understood. This study investigated the effects of AE on skeletal muscle in a MI model using Fndc5-/- and Alcat1- /- mice. The results showed that AE partially reversed the decreased expression of Irisin and antioxidant capacity, increased ALCAT1 expression, protein degradation, and cell apoptosis induced by MI. Knockout of Fndc5 further aggravated the oxidative stress and cell apoptosis in skeletal muscle, while knockout of Alcat1 reduced them and strengthened the beneficial effects of AE. In vitro experiments on C2C12 cells confirmed that Irisin and AICAR intervention inhibited ALCAT1 expression, oxidative stress, and cell apoptosis. These findings suggest that AE can alleviate oxidative stress and apoptosis in skeletal muscle following MI, partly through up-regulating Irisin and inhibiting ALCAT1 expression.
FREE RADICAL BIOLOGY AND MEDICINE
(2022)
Article
Biochemistry & Molecular Biology
Zhengye Liu, Thomas Chaillou, Estela Santos Alves, Theresa Mader, Baptiste Jude, Duarte M. S. Ferreira, Heidi Hynynen, Arthur J. Cheng, William O. Jonsson, Gianluigi Pironti, Daniel C. Andersson, Ellinor Kenne, Jorge L. Ruas, Pasi Tavi, Johanna T. Lanner
Summary: The study demonstrates that NDUFA4L2 regulates skeletal muscle mass and force by decreasing mitochondrial activity and production of reactive oxygen species, leading to muscle atrophy. Overexpression of NDUFA4L2 reduces mitochondrial respiration and antioxidant capacity, lowering levels of important intramuscular metabolites, ultimately affecting muscle function.
Review
Cell Biology
Han Dong, Shih-Yin Tsai
Summary: Mitochondria are crucial for energy production and play a vital role in various biological processes in eukaryotic cells. Skeletal muscle heavily relies on mitochondria for energy supplementation and also relies on them for maintaining calcium and reactive oxygen species levels. This review summarizes recent studies on mitochondria function and quality control in skeletal muscle, focusing on in vivo studies of rodents and human subjects. The interplay between mitochondrial functions and muscle fiber type-specific phenotypes, as well as the impact of aging and exercise on skeletal muscle and mitochondria properties, is also discussed.
Article
Biochemistry & Molecular Biology
Luz Marina Sanchez-Mendoza, Carlos Perez-Sanchez, Sandra Rodriguez-Lopez, Chary Lopez-Pedrera, Miguel Calvo-Rubio, Rafael de Cabo, Maria I. Buron, Jose A. Gonzalez-Reyes, Jose M. Villalba
Summary: The study investigates the effect of sex on metabolic adaptations induced by overexpression of CYB5R3 and the modulation of key markers related to mitochondrial function in skeletal muscle. It was found that CYB5R3 overexpression leads to enhanced mitochondrial biogenesis and function, as well as increased mitochondrial abundance in skeletal muscle. These beneficial actions are predominantly observed in females, with differences in NADH levels and the abundance of cytochrome c and DRP-1. The results also show ultrastructural changes in transgenic females, including an increase in the number and size of mitochondria.
FREE RADICAL BIOLOGY AND MEDICINE
(2023)
Review
Medicine, Research & Experimental
Colin Harper, Venkatesh Gopalan, Jorming Goh
Summary: This review examines the cellular and molecular changes in skeletal muscle mitochondria during aging, particularly focusing on the efficiency of mitochondrial coupling and its impact on muscle function decline. It also discusses how different exercise modalities can potentially reverse these changes and delay the onset of sarcopenia. Additional concepts such as mitophagy and the implications of muscle fiber type changes with sarcopenia on mitochondrial function are also integrated in this review.
JOURNAL OF TRANSLATIONAL MEDICINE
(2021)
Review
Pharmacology & Pharmacy
Yan Yan, Ming Li, Jie Lin, Yanan Ji, Kexin Wang, Dajun Yan, Yuntian Shen, Wei Wang, Zhongwei Huang, Haiyan Jiang, Hualin Sun, Lei Qi
Summary: This review summarizes the role of AMPK in regulating mitochondrial function and its impact on skeletal muscle metabolism and health.
FRONTIERS IN PHARMACOLOGY
(2022)
Article
Multidisciplinary Sciences
Joshua C. Drake, Rebecca J. Wilson, Rhianna C. Laker, Yuntian Guan, Hannah R. Spaulding, Anna S. Nichenko, Wenqing Shen, Huayu Shang, Maya Dorn, Kian Huang, Mei Zhang, Aloka B. Bandara, Matthew H. Brisendine, Jennifer A. Kashatus, Poonam R. Sharma, Alexander Young, Jitendra Gautam, Ruofan Cao, Horst Wallrabe, Paul A. Chang, Michael Wong, Eric M. Desjardins, Simon A. Hawley, George J. Christ, David F. Kashatus, Clint L. Miller, Matthew J. Wolf, Ammasi Periasamy, Gregory R. Steinberg, D. Grahame Hardie, Zhen Yan
Summary: Mitochondria form a complex, interconnected reticulum maintained through coordination among biogenesis, dynamic fission, fusion and mitophagy in response to various cues. Specific isoforms of AMP-activated protein kinase are localized on the outer mitochondrial membrane and vary in activation across the reticulum in response to energetic stress. The discovery highlights the complexity of sensing cellular energetics in vivo and its implications for targeting mitochondrial energetics in disease treatment.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2021)
Article
Multidisciplinary Sciences
Laura M. de Smalen, Anastasiya Borsch, Aurel B. Leuchtmann, Jonathan F. Gill, Danilo Ritz, Mihaela Zavolan, Christoph Handschin
Summary: Sarcopenia, the age-related loss of skeletal muscle mass and function, can significantly impact quality of life and mortality. This study found that mitochondrial proteostasis plays an important role in muscle aging and highlights the positive effects of exercise on mitochondrial protein synthesis.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2023)
Article
Geriatrics & Gerontology
Lisa Gambarotto, Samuele Metti, Martina Chrisam, Cristina Cerqua, Patrizia Sabatelli, Andrea Armani, Carlo Zanon, Marianna Spizzotin, Silvia Castagnaro, Flavie Strappazzon, Paolo Grumati, Matilde Cescon, Paola Braghetta, Eva Trevisson, Francesco Cecconi, Paolo Bonaldo
Summary: The study reveals that Ambra1 plays a critical role in the mitophagic flux of adult murine skeletal muscle and its deficiency leads to abnormal mitochondria and myofiber remodeling.
JOURNAL OF CACHEXIA SARCOPENIA AND MUSCLE
(2022)
Article
Cell Biology
HaiXu Song, Xiaoxiang Tian, Dan Liu, Meili Liu, Yanxia Liu, Jing Liu, Zhu Mei, Chenghui Yan, Yaling Han
Summary: The study established a skeletal muscle-specific CREG1 knockout mouse model, which showed effects on motor function and mitochondrial quality. Lack of CREG1 accelerated mitophagy in the skeletal muscle.
Article
Radiology, Nuclear Medicine & Medical Imaging
Benjamin Marty, Pierre-Yves Baudin, Ericky Caldas de Almeida Araujo, Yves Fromes, Karim Wahbi, Harmen Reyngoudt
Summary: This study used MR fingerprinting with water and fat separation to quantitatively evaluate skeletal muscle tissue alterations in patients with Becker muscular dystrophy. The results showed a significant increase in extracellular volume fraction (ECV) in the muscles of these patients, which was associated with fat fraction (FF) and water relaxation time quantification.
Article
Biochemistry & Molecular Biology
Yu Kitaoka
Summary: Nrf2 is believed to play a crucial role in protecting cells against oxidative stress and is also involved in energy metabolism. This review briefly discusses the role of Nrf2 in skeletal muscle metabolism from the perspective of exercise physiology.
Article
Biochemistry & Molecular Biology
Baojun Sun, Hitomi Maruta, Yun Ma, Hiromi Yamashita
Summary: Taurine is an abundant free amino acid in mammalian tissues that plays a role in skeletal muscle function and exercise capacity. This study investigated the mechanism of taurine function in skeletal muscles by examining the effects of short-term administration of taurine on rats and L6 cells. The results suggest that taurine modulates skeletal muscle function by activating AMP-activated protein kinase through the calcium signaling pathway, leading to the expression of genes and proteins associated with mitochondrial and respiratory metabolism.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Medicine, Research & Experimental
Stephanie E. Hall, Bumsoo Ahn, Ashley J. Smuder, Aaron B. Morton, J. Matthew Hinkley, Michael P. Wiggs, Kurt J. Sollanek, Hayden Hyatt, Scott K. Powers
Summary: Mechanical ventilation is a life-saving intervention, but can lead to inspiratory muscle weakness over time. Research suggests blocking angiotensin II type 1 receptors may protect against this weakness. Comparing two ARBs, irbesartan and olmesartan, it was found that olmesartan is more effective in protecting against VIDD, providing a potential future therapy.
CTS-CLINICAL AND TRANSLATIONAL SCIENCE
(2021)
Article
Biochemistry & Molecular Biology
Rizwan Qaisar, Gavin Pharaoh, Shylesh Bhaskaran, Hongyang Xu, Rojina Ranjit, Jan Bian, Bumsoo Ahn, Constantin Georgescu, Jonathan D. Wren, Holly Van Remmen
Summary: The study showed that pharmacological activation of SERCA can mitigate sarcopenia phenotype in aging mice, reversing reductions in muscle mass and force generation, and preventing an increase in mitochondrial ROS production. These effects are mediated in part by enhanced cellular energetics through activation of PGC1-alpha, UCP1, HSF1, and APMK, as well as increased regenerative capacity by suppression of MEF2C and p38 MAPK signaling.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Medicine, Research & Experimental
Trace Thome, Ravi A. Kumar, Sarah K. Burke, Ram B. Khattri, Zachary R. Salyers, Rachel C. Kelley, Madeline D. Coleman, Demetra D. Christou, Russell T. Hepple, Salvatore T. Scali, Leonardo F. Ferreira, Terence E. Ryan
Summary: This study investigated the mechanisms of skeletal muscle mitochondrial impairment in mice with adenine-induced CKD. It found reductions in mitochondrial oxidative phosphorylation and identified unknown uremic metabolites associated with the degree of mitochondrial impairment. Additionally, CKD mice showed muscle atrophy, protein degradation, and morphological changes in the neuromuscular junction.
Article
Genetics & Heredity
Svetlana Yegorova, Oleg Yegorov, Leonardo F. Ferreira
Summary: The study identified 112 differentially expressed genes in the diaphragm post-chronic myocardial infarction, suggesting pathological remodeling and potential biological targets related to neuromuscular junction, extracellular matrix, metabolism and iron homeostasis.
Review
Geriatrics & Gerontology
Brady J. Holmer, Stephanie S. Lapierre, Danielle E. Jake-Schoffman, Demetra D. Christou
Summary: Sleep deprivation is associated with increased cardiovascular disease (CVD) morbidity and mortality, with age-related alterations potentially exacerbating CVD susceptibility in older individuals. Endothelial dysfunction may play a central role in linking sleep deprivation to CVD, although the exact mechanisms are not fully understood.
Article
Physiology
Orlando Laitano, Jose Pindado, Isela Valera, Ray A. Spradlin, Kevin O. Murray, Katelyn R. Villani, Jamal M. Alzahrani, Terence E. Ryan, Philip A. Efron, Leonardo F. Ferreira, Elisabeth R. Barton, Thomas L. Clanton
Summary: The combination of sepsis and hindlimb disuse models in mice induces muscle dysfunction and immune cell infiltration in a muscle-dependent manner, highlighting the importance of rehabilitative interventions in septic hosts to prevent muscle disuse and attenuate myopathy.
PHYSIOLOGICAL REPORTS
(2021)
Article
Physiology
Rachel C. Kelley, Lauren Betancourt, Andrea M. Noriega, Suzanne C. Brinson, Nuria Curbelo-Bermudez, Dongwoo Hahn, Ravi A. Kumar, Eliza Balazic, Derek R. Muscato, Terence E. Ryan, Robbert J. van der Pijl, Shengyi Shen, Coen A. C. Ottenheijm, Leonardo F. Ferreira
Summary: Heart failure with preserved ejection fraction (HFpEF) is highly prevalent in postmenopausal women and is characterized by specific features such as skeletal myopathy. A new rat model of postmenopausal HFpEF was developed and it exhibited cardiovascular and systemic abnormalities similar to the human disease. The study found that the skeletal myopathy of postmenopausal HFpEF involves decreased muscle force, mitochondrial dysfunction, and oxidative imbalance.
JOURNAL OF APPLIED PHYSIOLOGY
(2022)
Article
Cell Biology
Bumsoo Ahn, Rojina Ranjit, Parker Kneis, Hongyang Xu, Katarzyna M. Piekarz, Willard M. Freeman, Michael Kinter, Arlan Richardson, Qitao Ran, Susan V. Brooks, Holly Van Remmen
Summary: The study aimed to determine the impact of mitochondrial hydrogen peroxide on muscle aging and contractile dysfunction. Results showed that muscle-specific overexpression of mPRDX3 can reduce mitochondrial H2O2 generation, improve mitochondrial function, and mitigate loss of muscle quantity and quality, despite the persistence of neuromuscular junction impairment.
Article
Physiology
Ryan J. Pettit-Mee, Gavin Power, Francisco J. Cabral-Amador, Francisco Ramirez-Perez, Rogerio N. Soares, Neekun Sharma, Ying Liu, Demetra D. Christou, Jill A. Kanaley, Luis A. Martinez-Lemus, Camila Manrique-Acevedo, Jaume Padilla
Summary: The reduced expression of heat shock protein 72 (HSP72) is not a key driver of endothelial insulin resistance in type 2 diabetes. Lower-body heating may be an effective strategy for improving leg blood flow responses to glucose ingestion-induced hyperinsulinemia.
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Ravi Kumar, Andrew R. Coggan, Leonardo F. Ferreira
Summary: Nitric oxide (NO) is a complex modulator of skeletal muscle contractile function, with the ability to increase or decrease force and power output depending on various factors. The effects of NO on contractile function may be dose-dependent and have fiber type and sex specificity, potentially mediated by post-translational modifications of myofibrillar proteins.
NITRIC OXIDE-BIOLOGY AND CHEMISTRY
(2022)
Article
Physiology
Rachel C. Kelley, Stephanie S. Lapierre, Derek R. Muscato, Dongwoo Hahn, Demetra D. Christou, Leonardo F. Ferreira
Summary: This study found that a high-fat, high-sucrose diet induces cardiac dysfunction but does not affect the diaphragm in male rats. Supplementation with the antioxidant N-acetylcysteine can attenuate the cardiac abnormalities caused by this diet. This research is important for understanding the cardiovascular dysfunction caused by obesity and the therapeutic potential of antioxidants.
EXPERIMENTAL PHYSIOLOGY
(2022)
Article
Cell Biology
Ravi A. Kumar, Trace Thome, Omar M. Sharaf, Terence E. Ryan, George J. Arnaoutakis, Eric Jeng, Leonardo F. Ferreira
Summary: Cardiomyocyte dysfunction in patients with end-stage heart failure with reduced ejection fraction is associated with mitochondrial dysfunction. Reversible thiol oxidation can modulate mitochondrial function, but other components of mitochondrial energy transfer are limiting factors in end-stage heart failure.
Article
Multidisciplinary Sciences
Hongyang Xu, Bumsoo Ahn, Holly Van Remmen
Summary: Aging and oxidative stress have specific impacts on mechanisms related to muscle weakness, including reduced membrane excitability, altered signaling and stability, decreased Ca2+ sensitivity, modified SERCA activity, disrupted Ca2+ homeostasis, and impaired mitochondrial function.
Review
Public, Environmental & Occupational Health
Kellie B. Cooper, Stephanie Lapierre, Montserrat Carrera Seoane, Katie Lindstrom, Ricarda Pritschmann, Marissa Donahue, Demetra D. Christou, Megan A. McVay, Danielle E. Jake-Schoffman
Summary: The common behavior change techniques in digital physical activity interventions for breast cancer survivors include goal setting, social support, and self-monitoring. However, many potentially effective behavior change techniques are underutilized and should be considered for future interventions. Rating: 7/10
TRANSLATIONAL BEHAVIORAL MEDICINE
(2023)
Article
Biochemistry & Molecular Biology
Rojina Ranjit, Holly Van Remmen, Bumsoo Ahn
Summary: Sarcopenia, the progressive loss of muscle mass and dysfunction, affects the elderly and has negative effects on their quality of life. However, no pharmacological therapies are currently available for this condition. Recent studies have shown that ghrelin, a gut-released hormone, has protective effects on skeletal muscle. In this study, it was found that unacylated ghrelin can reduce muscle atrophy and contractile dysfunction.
