{"title":"Muscle spindle receptors and their impact on Parkinson´s disease and Cerebral Palsy subjects.","authors":"Else Marie Bartels, Adrian Harrison","doi":"10.1007/s10974-024-09682-8","DOIUrl":"https://doi.org/10.1007/s10974-024-09682-8","url":null,"abstract":"<p><p>In some neurological conditions, like Parkinson's disease (PD) and Cerebral Palsy (CP), as well as with ageing, muscle spindles have been mentioned as participating in the pathological response of observed muscles. The aim of this review has therefore been to examine what is known about muscle spindle receptors, their function and how they are involved in regulating precise muscle movement in relation to these two conditions. Data from acoustic myography (AMG) studies with healthy controls (HC), CP and PD subjects have been re-examined with a view to identifying possible effects of changes in muscle movement which could be related to muscle spindle receptor function. Studies of muscle spindles have shown that during shortening and lengthening contractions the fusimotor system is activated differently with different discharge frequencies and sensitivities. With increasing age comes a loss of precise proprioception, something that coincides with a change in the AMG E-score towards lower values, indicating a reduced level of coordination and efficiency of muscle use. With PD and CP there is likewise a documented decrease in proprioception, also showing lower E-values than age-matched HC subjects. We conclude that the decrease in proprioception observed in these subjects must be partly due to a change in the muscle spindle / C-centre feedback system.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142622141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Unraveling the bidirectional relationship between muscle inflammation and satellite cells activity: influencing factors and insights.","authors":"Esmail Karami, Behzad Bazgir, Hossein Shirvani, Mohammad Taghi Mohammadi, Mansoor Khaledi","doi":"10.1007/s10974-024-09683-7","DOIUrl":"https://doi.org/10.1007/s10974-024-09683-7","url":null,"abstract":"<p><p>Inflammation stands as a vital and innate function of the immune system, essential for maintaining physiological homeostasis. Its role in skeletal muscle regeneration is pivotal, with the activation of satellite cells (SCs) driving the repair and generation of new myofibers. However, the relationship between inflammation and SCs is intricate, influenced by various factors. Muscle injury and repair prompt significant infiltration of immune cells, particularly macrophages, into the muscle tissue. The interplay of cytokines and chemokines from diverse cell types, including immune cells, fibroadipogenic progenitors, and SCs, further shapes the inflammation-SCs dynamic. While some studies suggest heightened inflammation associates with reduced SC activity and increased fibro- or adipogenesis, others indicate an inflammatory stimulus benefits SC function. Yet, the existing literature struggles to delineate clearly between the stimulatory and inhibitory effects of inflammation on SCs and muscle regeneration. This paper comprehensively reviews studies exploring the impact of pharmacological agents, dietary interventions, genetic factors, and exercise regimes on the interplay between inflammation and SC activity.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142604288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The 50th anniversary of the European Society for Muscle Research: a journey through half a century of scientific advances.","authors":"Ger Stienen, Carlo Reggiani","doi":"10.1007/s10974-024-09666-8","DOIUrl":"10.1007/s10974-024-09666-8","url":null,"abstract":"<p><p>The European Society for Muscle Research (ESMR) started in 1971 as \"European Muscle Club\" in a joint initiative of Marcus Schaub, Eduard Jenny and Rudolf Billeter (Zurich), Caspar Rüegg (Heidelberg), Jean Légér (Montpellier), Bernard Swynghedauw (Paris), George Maréchal (Brussels), Gabriel Hamoir (Liège), and Endre Biró (Budapest). Since 1972, local organizers took care of muscle conferences held yearly in different European countries and in Israel in 1987. One of the goals was to establish contacts and collaborations between scientists on both sides of the Iron Curtain. Starting as an informal club, enthusiastically guided by Marcus Schaub as secretary (1971-1995) and later by Ger Stienen (1996-2005), Anders Arner (2006-2017) and Wolfgang Linke (2018-), the ESMR meetings steered international collaborations. The meetings witnessed the remarkable advancement of the insight in skeletal, smooth and cardiac muscle structure and function. In the five decades, the thin and thick filament structure has been resolved to the atomic level, the mechanism of acto-myosin energy transduction and force generation as well as its regulation have been elucidated. The molecular basis of striated and smooth muscle diversity has been found in the existence of multiple protein isoforms. The transcriptional, translational and post-translational regulations which give rise to adaptive responses of muscle tissue have been revealed. Many new players entered the field, such as titin, the ryanodine receptor and several signalling factors. Substantial progress has also been made in the identification of the pathogenesis of many hereditary muscle diseases such as Duchenne MuscularDystrophy and Hypertrophic Cardiac Myopathies.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":" ","pages":"87-94"},"PeriodicalIF":1.8,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139729840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anja Vidović, Klemen Dolinar, Alexander V Chibalin, Sergej Pirkmajer
{"title":"AMPK and glucose deprivation exert an isoform-specific effect on the expression of Na<sup>+</sup>,K<sup>+</sup>-ATPase subunits in cultured myotubes.","authors":"Anja Vidović, Klemen Dolinar, Alexander V Chibalin, Sergej Pirkmajer","doi":"10.1007/s10974-024-09673-9","DOIUrl":"10.1007/s10974-024-09673-9","url":null,"abstract":"<p><p>In skeletal muscle, Na<sup>+</sup>,K<sup>+</sup>-ATPase (NKA), a heterodimeric (α/β) P-type ATPase, has an essential role in maintenance of Na<sup>+</sup> and K<sup>+</sup> homeostasis, excitability, and contractility. AMP-activated protein kinase (AMPK), an energy sensor, increases the membrane abundance and activity of NKA in L6 myotubes, but its potential role in regulation of NKA content in skeletal muscle, which determines maximum capacity for Na<sup>+</sup> and K<sup>+</sup> transport, has not been clearly delineated. We examined whether energy stress and/or AMPK affect expression of NKA subunits in rat L6 and primary human myotubes. Energy stress, induced by glucose deprivation, increased protein content of NKAα1 and NKAα2 in L6 myotubes, while decreasing the content of NKAα1 in human myotubes. Pharmacological AMPK activators (AICAR, A-769662, and diflunisal) modulated expression of NKA subunits, but their effects only partially mimicked those that occurred in response to glucose deprivation, indicating that AMPK does not mediate all effects of energy stress on NKA expression. Gene silencing of AMPKα1/α2 increased protein levels of NKAα1 in L6 myotubes and NKAα1 mRNA levels in human myotubes, while decreasing NKAα2 protein levels in L6 myotubes. Collectively, our results suggest a role for energy stress and AMPK in modulation of NKA expression in skeletal muscle. However, their modulatory effects were not conserved between L6 myotubes and primary human myotubes, which suggests that coupling between energy stress, AMPK, and regulation of NKA expression in vitro depends on skeletal muscle cell model.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":" ","pages":"139-154"},"PeriodicalIF":1.8,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11316707/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140863275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Peter O Awinda, Blake J Vander Top, Kyrah L Turner, Bertrand C W Tanner
{"title":"Danicamtiv affected isometric force and cross-bridge kinetics similarly in skinned myocardial strips from male and female rats.","authors":"Peter O Awinda, Blake J Vander Top, Kyrah L Turner, Bertrand C W Tanner","doi":"10.1007/s10974-024-09669-5","DOIUrl":"10.1007/s10974-024-09669-5","url":null,"abstract":"<p><p>Myotropes are pharmaceuticals that have recently been developed or are under investigation for the treatment of heart diseases. Myotropes have had varied success in clinical trials. Initial research into myotropes have widely focused on animal models of cardiac dysfunction in comparison with normal animal cardiac physiology-primarily using males. In this study we examined the effect of danicamtiv, which is one type of myotrope within the class of myosin activators, on contractile function in permeabilized (skinned) myocardial strips from male and female Sprague-Dawley rats. We found that danicamtiv increased steady-state isometric force production at sub-maximal calcium levels, leading to greater Ca<sup>2+</sup>-sensitivity of contraction for both sexes. Danicamtiv did not affect maximal Ca<sup>2+</sup>-activated force for either sex. Sinusoidal length-perturbation analysis was used to assess viscoelastic myocardial stiffness and cross-bridge cycling kinetics. Data from these measurements did not vary with sex, and the data suggest that danicamtiv slows cross-bridge cycling kinetics. These findings imply that danicamtiv increases force production via increasing cross-bridge contributions to activation of contraction, especially at sub-maximal Ca<sup>2+</sup>-activation. The inclusion of both sexes in animal models during the formative stages of drug development could be helpful for understanding the efficacy or limitation of a drug's therapeutic impact on cardiac function.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":" ","pages":"115-122"},"PeriodicalIF":1.8,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140876595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Blaž Kociper, Nives Škorja Milić, Ivana Ogrizek, Katarina Miš, Sergej Pirkmajer
{"title":"Inhibition of the ubiquitin-proteasome system reduces the abundance of pyruvate dehydrogenase kinase 1 in cultured myotubes.","authors":"Blaž Kociper, Nives Škorja Milić, Ivana Ogrizek, Katarina Miš, Sergej Pirkmajer","doi":"10.1007/s10974-024-09679-3","DOIUrl":"10.1007/s10974-024-09679-3","url":null,"abstract":"<p><p>Pyruvate dehydrogenase kinase (PDK), which phosphorylates the pyruvate dehydrogenase complex, regulates glucose metabolism in skeletal muscle. PDK1, an isozyme whose expression is controlled by hypoxia-inducible factor-1α (HIF-1α), is thought to play a role in muscle adaptation to hypoxia. While transcriptional upregulation of PDK1 by HIF-1α is well characterised, mechanisms controlling proteolysis of PDK1 in skeletal muscle have not been thoroughly investigated. Proteasome inhibitor MG132 paradoxically reduced the abundance of PDK1 in human cancer cells and rat L6 myotubes, suggesting that MG132 might direct PDK1 towards autophagic degradation. The objectives of our current study were to determine (1) whether MG132 suppresses PDK1 levels in primary human myotubes, (2) whether chloroquine, an inhibitor of autophagy, prevents MG132-induced suppression of PDK1 in L6 myotubes, and (3) whether PYR-41, an inhibitor of ubiquitination, suppresses PDK1 in L6 myotubes. Using qPCR and/or immunoblotting, we found that despite markedly upregulating HIF-1α protein, MG132 did not alter the PDK1 expression in cultured primary human myotubes, while it suppressed both PDK1 mRNA and protein in L6 myotubes. The PDK1 levels in L6 myotubes were suppressed also during co-treatment with chloroquine and MG132. PYR-41 markedly increased the abundance of HIF-1α in primary human and L6 myotubes, while reducing the abundance of PDK1. In L6 myotubes treated with PYR-41, chloroquine increased the abundance of the epidermal growth factor receptor, but did not prevent the suppression of PDK1. Collectively, our results suggest that cultured myotubes degrade PDK1 via a pathway that cannot be inhibited by MG132, PYR-41, and/or chloroquine.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":" ","pages":"155-169"},"PeriodicalIF":1.8,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11316709/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141855836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Dana Cizkova, Jitka M Zurmanova, Lucie Gerykova, Alexandros Kouvelas, Mario Heles, Barbara Elsnicova, Frantisek Galatik, Jan Silhavy, Michal Pravenec, Jaroslav Mokry
{"title":"Nestin expression in intact and hypertrophic myocardium of spontaneously hypertensive rats during aging.","authors":"Dana Cizkova, Jitka M Zurmanova, Lucie Gerykova, Alexandros Kouvelas, Mario Heles, Barbara Elsnicova, Frantisek Galatik, Jan Silhavy, Michal Pravenec, Jaroslav Mokry","doi":"10.1007/s10974-023-09641-9","DOIUrl":"10.1007/s10974-023-09641-9","url":null,"abstract":"<p><p>Nestin is a unique intermediate filament expressed for a short period in the developing heart. It was also documented in several cell types of the adult myocardium under pathological conditions such as myocardial infarction or fibrosis. However, circumstances of nestin re-occurrence in the diseased or aging heart have not been elucidated yet. In this work we immunohistochemically detected nestin to determine its expression and distribution pattern in the left ventricular myocardium of normotensive Wistar Kyoto (WKY) rats and in the hypertrophic ones of spontaneously hypertensive (SHR) rats, both at the age of 1 and 1.5 year. No nestin<sup>+</sup> cells were identified in the intact myocardium of 1-year-old WKY rats, whereas in the aged 1.5-year-old WKY rats nestin<sup>+</sup> endothelial cells in some blood vessels were discovered. In the hypertrophic myocardium of all SHR rats, nestin was rarely detected in desmin<sup>+</sup> vimentin<sup>-</sup> cardiomyocytes and in some vimentin<sup>+</sup> interstitial cells often accumulated in clusters, varying in intensity of desmin immunoreactivity. Moreover, nestin was infrequently expressed in the endothelial cells of some myocardial blood vessels in 1-year-old SHR rats, but not in 1.5-year-old ones. Quantitative image analysis of nestin expression in the myocardium confirmed significant increase in 1.5-year-old WKY rats and in SHR rats of both ages compared to the intact 1-year-old WKY rats. This study firstly documents nestin re-expression indicating cytoskeletal remodelling in different cell types of the aging intact and chronically pressure over-loaded hypertrophied myocardium. Our findings confirm nestin involvement in complex changes during myocardial hypertrophy and progressive aging.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":" ","pages":"41-51"},"PeriodicalIF":1.8,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11096222/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9176502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mi Jin Kim, Ji Min Lee, Kyunghoon Min, Yong-Soo Choi
{"title":"Xenogeneic transplantation of mitochondria induces muscle regeneration in an in vivo rat model of dexamethasone-induced atrophy.","authors":"Mi Jin Kim, Ji Min Lee, Kyunghoon Min, Yong-Soo Choi","doi":"10.1007/s10974-023-09643-7","DOIUrl":"10.1007/s10974-023-09643-7","url":null,"abstract":"<p><p>Muscle atrophy significantly impairs health and quality of life; however, there is still no cure. Recently, the possibility of regeneration in muscle atrophic cells was suggested through mitochondrial transfer. Therefore, we attempted to prove the efficacy of mitochondrial transplantation in animal models. To this end, we prepared intact mitochondria from umbilical cord-derived mesenchymal stem cells maintaining their membrane potential. To examine the efficacy of mitochondrial transplantation on muscle regeneration, we measured muscle mass, cross-sectional area of muscle fiber, and changes in muscle-specific protein. In addition, changes in the signaling mechanisms related to muscle atrophy were evaluated. As a result, in mitochondrial transplantation, the muscle mass increased by 1.5-fold and the lactate concentration decreased by 2.5-fold at 1 week in dexamethasone-induced atrophic muscles. In addition, a 2.3-fold increase in the expression of desmin protein, a muscle regeneration marker, showed a significant recovery in MT 5 µg group. Importantly, the muscle-specific ubiquitin E3-ligases MAFbx and MuRF-1 were significantly decreased through AMPK-mediated Akt-FoxO signaling pathway by mitochondrial transplantation compared with the saline group, reaching a level similar to that in the control. Based on these results, mitochondrial transplantation may have therapeutic applications in the treatment of atrophic muscle disorders.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":" ","pages":"53-68"},"PeriodicalIF":2.7,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10748928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Michael A. Lopez, Patricia S. Pardo, Junaith S. Mohamed, Aladin M. Boriek
{"title":"ANKRD1 expression is aberrantly upregulated in the mdm mouse model of muscular dystrophy and induced by stretch through NFκB","authors":"Michael A. Lopez, Patricia S. Pardo, Junaith S. Mohamed, Aladin M. Boriek","doi":"10.1007/s10974-024-09671-x","DOIUrl":"https://doi.org/10.1007/s10974-024-09671-x","url":null,"abstract":"<p>The muscular dystrophy with myositis (<i>mdm)</i> mouse model results in a severe muscular dystrophy due to an 83-amino-acid deletion in the N2A region of titin, an expanded sarcomeric protein that functions as a molecular spring which senses and modulates the response to mechanical forces in cardiac and skeletal muscles. ANKRD1 is one of the muscle ankyrin repeat domain proteins (MARPs) a family of titin-associated, stress-response molecules and putative transducers of stretch-induced signaling in skeletal muscle. The aberrant over-activation of Nuclear factor Kappa B (NF-κB) and the Ankyrin-repeat domain containing protein 1 (ANKRD1) occurs in several models of progressive muscle disease including Duchenne muscular dystrophy. We hypothesized that mechanical regulation of ANKRD1 is mediated by NF-κB activation in skeletal muscles and that this mechanism is perturbed by small deletion of the stretch-sensing titin N2A region in the <i>mdm</i> mouse. We applied static mechanical stretch of the <i>mdm</i> mouse diaphragm and cyclic mechanical stretch of C<sub>2</sub>C<sub>12</sub> myotubes to examine the interaction between NF−κΒ and ANKRD1 expression utilizing Western blot and qRTPCR. As seen in skeletal muscles of other severe muscular dystrophies, an aberrant increased basal expression of NF-κB and ANKRD1 were observed in the diaphragm muscles of the <i>mdm</i> mice. Our data show that in the <i>mdm</i> diaphragm, basal levels of NF-κB are increased, and pharmacological inhibition of NF-κB does not alter basal levels of ANKRD1. Alternatively, NF-κB inhibition did alter stretch-induced ANKRD1 upregulation. These data show that NF-κB activity is at least partially responsible for the stretch-induced expression of ANKRD1.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":"10 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140836400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Arginine ingestion inhibits phagocyte invasion in eccentrically contracted rat fast-twitch muscle","authors":"Keita Kanzaki, Masanobu Wada","doi":"10.1007/s10974-024-09672-w","DOIUrl":"https://doi.org/10.1007/s10974-024-09672-w","url":null,"abstract":"<p>Eccentric contraction (ECC) has been shown to induce leukocyte invasion into skeletal muscle, resulting in muscle inflammation. This study aimed to investigate whether prior ingestion of <span>L</span>-arginine (ARG), a nitric oxide precursor, inhibits ECC-induced macrophage invasion. Male Wistar rats received ARG in water for 7 days, beginning 3 days prior to ECC. ECCs were induced in the anterior crural muscles for 200 cycles. Three days later, the tibialis anterior and extensor digitorum longus muscles were excised for biochemical analysis and force measurement, respectively. ARG ingestion increased nitrite and nitrate levels in plasma and muscle, inhibiting force depression and reducing CD68 content in muscles subjected to ECC. ARG ingestion also ameliorated an ECC-induced increase in protein nitration, although neither ARG ingestion nor ECC induction affected protein carbonyl levels. The present results suggest that ingestion of ARG or ARG-rich foods may alleviate inflammation by attenuating phagocyte invasion in eccentrically contracted skeletal muscles.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":"213 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140627773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}