{"title":"Blood endothelium transition and phenotypic plasticity: A key regulator of integrity/permeability in response to ischemia","authors":"Nicolas Bréchot , Alexandre Rutault , Iris Marangon , Stéphane Germain","doi":"10.1016/j.semcdb.2023.07.004","DOIUrl":"10.1016/j.semcdb.2023.07.004","url":null,"abstract":"<div><p>In the human body, the 10<sup>13</sup> blood endothelial cells (ECs) which cover a surface of 500–700 m<sup>2</sup> (Mai et al., 2013) are key players of tissue homeostasis, remodeling and regeneration. Blood vessel ECs play a major role in the regulation of metabolic and gaz exchanges, cell trafficking, blood coagulation, vascular tone, blood flow and fluid extravasation (also referred to as blood vascular permeability). ECs are heterogeneous in various capillary beds and have the exquisite capacity to cope with environmental changes by regulating their gene expression. Ischemia has major detrimental effects on the endothelium and ischemia-induced regulation of vascular integrity is of paramount importance for human health, as small amounts of fluid accumulation in the interstitium may be responsible for major effects on organ functions and patients outcome. In this review, we will here focus on the stimuli and the molecular mechanisms that control blood endothelium maintenance and phenotypic plasticity/transition involved in controlling blood capillary leakage that might open new avenues for therapeutic applications.</p></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"155 ","pages":"Pages 16-22"},"PeriodicalIF":7.3,"publicationDate":"2023-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9905386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Death and survival from executioner caspase activation","authors":"Gongping Sun","doi":"10.1016/j.semcdb.2023.07.005","DOIUrl":"10.1016/j.semcdb.2023.07.005","url":null,"abstract":"<div><p>Executioner caspases<span> are evolutionarily conserved regulators of cell death under apoptotic stress. Activated executioner caspases drive apoptotic cell death through cleavage of diverse protein substrates or pyroptotic cell death in the presence of gasdermin E. On the other hand, activation of executioner caspases can also trigger pro-survival and pro-proliferation signals. In recent years, a growing body of studies have demonstrated that cells can survive from executioner caspase activation in response to stress and that the survivors undergo molecular and phenotypic alterations. This review focuses on death and survival from executioner caspase activation, summarizing the role of executioner caspases in apoptotic and pyroptotic cell death and discussing the potential mechanism and consequences of survival from stress-induced executioner caspase activation.</span></p></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"156 ","pages":"Pages 66-73"},"PeriodicalIF":7.3,"publicationDate":"2023-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10195802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Brendon J. Gurd , Eveline Soares Menezes , Benjamin B. Arhen , Hashim Islam
{"title":"Impacts of altered exercise volume, intensity, and duration on the activation of AMPK and CaMKII and increases in PGC-1α mRNA","authors":"Brendon J. Gurd , Eveline Soares Menezes , Benjamin B. Arhen , Hashim Islam","doi":"10.1016/j.semcdb.2022.05.016","DOIUrl":"10.1016/j.semcdb.2022.05.016","url":null,"abstract":"<div><p><span><span>The purpose of this review is to explore and discuss the impacts of augmented training volume, intensity, and duration on the phosphorylation/activation of key signaling protein – AMPK, CaMKII and PGC-1α - involved in the initiation of </span>mitochondrial biogenesis. Specifically, we explore the impacts of augmented exercise protocols on AMP/ADP and Ca</span><sup>2+</sup> signaling and changes in post exercise PGC − 1α gene expression. Although AMP/ADP concentrations appear to increase with increasing intensity and during extended durations of higher intensity exercise AMPK activation results are varied with some results supporting and intensity/duration effect and others not. Similarly, CaMKII activation and signaling results following exercise of different intensities and durations are inconsistent. The PGC-1α literature is equally inconsistent with only some studies demonstrating an effect of intensity on post exercise mRNA expression. We present a novel meta-analysis that suggests that the inconsistency in the PGC-1α literature may be due to sample size and statistical power limitations owing to the effect of intensity on PGC-1α expression being small. There is little data available regarding the impact of exercise duration on PGC-1α expression. We highlight the need for future well designed, adequately statistically powered, studies to clarify our understanding of the effects of volume, intensity, and duration on the induction of mitochondrial biogenesis by exercise.</p></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"143 ","pages":"Pages 17-27"},"PeriodicalIF":7.3,"publicationDate":"2023-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9189286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anna Picca , Flora Guerra , Riccardo Calvani , Roberta Romano , Hélio José Coelho-Junior , Cecilia Bucci , Christiaan Leeuwenburgh , Emanuele Marzetti
{"title":"Mitochondrial-derived vesicles in skeletal muscle remodeling and adaptation","authors":"Anna Picca , Flora Guerra , Riccardo Calvani , Roberta Romano , Hélio José Coelho-Junior , Cecilia Bucci , Christiaan Leeuwenburgh , Emanuele Marzetti","doi":"10.1016/j.semcdb.2022.03.023","DOIUrl":"10.1016/j.semcdb.2022.03.023","url":null,"abstract":"<div><p><span><span>Mitochondrial remodeling is crucial to meet the bioenergetic demand to support muscle contractile activity during daily tasks and </span>muscle regeneration following injury. A set of mitochondrial quality control (MQC) processes, including </span>mitochondrial biogenesis<span>, dynamics, and mitophagy<span>, are in place to maintain a well-functioning mitochondrial network and support muscle regeneration. Alterations in any of these pathways compromises mitochondrial quality and may potentially lead to impaired myogenesis, defective muscle regeneration, and ultimately loss of muscle function.</span></span></p><p>Among MQC processes, mitophagy has gained special attention for its implication in the clearance of dysfunctional mitochondria via crosstalk with the endo-lysosomal system, a major cell degradative route. Along this pathway, additional opportunities for mitochondrial disposal have been identified that may also signal at the systemic level. This communication occurs via inclusion of mitochondrial components within membranous shuttles named mitochondrial-derived vesicles (MDVs).</p><p>Here, we discuss MDV generation and release as a mitophagy-complementing route for the maintenance of mitochondrial homeostasis in skeletal myocytes. We also illustrate the possible role of muscle-derived MDVs in immune signaling during muscle remodeling and adaptation.</p></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"143 ","pages":"Pages 37-45"},"PeriodicalIF":7.3,"publicationDate":"2023-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9248063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jessica R. Dent , Ben Stocks , Dean G. Campelj , Andrew Philp
{"title":"Transient changes to metabolic homeostasis initiate mitochondrial adaptation to endurance exercise","authors":"Jessica R. Dent , Ben Stocks , Dean G. Campelj , Andrew Philp","doi":"10.1016/j.semcdb.2022.03.022","DOIUrl":"10.1016/j.semcdb.2022.03.022","url":null,"abstract":"<div><p><span>Endurance exercise is well established to increase mitochondrial content and function in skeletal muscle, a process termed </span>mitochondrial biogenesis<span><span>. Current understanding is that exercise initiates skeletal muscle mitochondrial remodeling via modulation of cellular nutrient, energetic and contractile stress pathways. These subtle changes in the cellular milieu are sensed by numerous transduction pathways that serve to initiate and coordinate an increase in mitochondrial gene transcription and translation. The result of these acute signaling events is the promotion of growth and assembly of mitochondria, coupled to a greater capacity for aerobic ATP provision in skeletal muscle. The aim of this review is to highlight the acute metabolic events induced by endurance exercise and the subsequent molecular pathways that sense this transient change in cellular </span>homeostasis to drive mitochondrial adaptation and remodeling.</span></p></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"143 ","pages":"Pages 3-16"},"PeriodicalIF":7.3,"publicationDate":"2023-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9563145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Mitochondrial Apoptotic Signaling Involvement in Remodeling During Myogenesis and Skeletal Muscle Atrophy","authors":"Fasih Ahmad Rahman, Joe Quadrilatero","doi":"10.1016/j.semcdb.2022.01.011","DOIUrl":"10.1016/j.semcdb.2022.01.011","url":null,"abstract":"<div><p>Mitochondria play a major role in apoptotic signaling. In addition to its role in eliminating dysfunctional cells, mitochondrial apoptotic signaling is implicated as a key component of myogenic differentiation and skeletal muscle atrophy. For example, the activation of cysteine-aspartic proteases (caspases; CASP's) can aid in the initial remodeling stages of myogenic differentiation by cleaving protein kinases, transcription factors, and cytoskeletal proteins<span>. Precise regulation of these signals is needed to prevent excessive cell disassemble and subsequent cell death. During skeletal muscle atrophy, the activation of CASP's and mitochondrial derived nucleases<span> participate in myonuclear fragmentation, a potential loss of myonuclei, and cleavage of contractile structures within skeletal muscle. The B cell leukemia/lymphoma 2 (BCL2) family of proteins play a significant role in regulating myogenesis and skeletal muscle atrophy by governing the initiating steps of mitochondrial apoptotic signaling. This review discusses the role of mitochondrial apoptotic signaling in skeletal muscle remodeling during myogenic differentiation and skeletal muscle pathological states, including aging, disuse, and muscular dystrophy.</span></span></p></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"143 ","pages":"Pages 66-74"},"PeriodicalIF":7.3,"publicationDate":"2023-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9253601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Emerging role of mitophagy in myoblast differentiation and skeletal muscle remodeling","authors":"Fasih Ahmad Rahman, Joe Quadrilatero","doi":"10.1016/j.semcdb.2021.11.026","DOIUrl":"10.1016/j.semcdb.2021.11.026","url":null,"abstract":"<div><p><span>Mitochondrial turnover in the form of </span>mitophagy<span> is emerging as a central process in maintaining cellular function. The degradation of damaged mitochondria through mitophagy is particularly important in cells/tissues that exhibit high energy demands. Skeletal muscle is one such tissue that requires precise turnover of mitochondria in several conditions in order to optimize energy production and prevent bioenergetic<span> crisis. For instance, the formation of skeletal muscle (i.e., myogenesis) is accompanied by robust turnover of low-functioning mitochondria to eventually allow the formation of high-functioning mitochondria. In mature skeletal muscle, alterations in mitophagy-related signaling occur during exercise, aging, and various disease states. Nonetheless, several questions regarding the direct role of mitophagy in various skeletal muscle conditions remain unknown. Furthermore, given the heterogenous nature of skeletal muscle with respect to various cellular and molecular properties, and the plasticity in these properties in various conditions, the involvement and characterization of mitophagy requires more careful consideration in this tissue. Therefore, this review will highlight the known mechanisms of mitophagy in skeletal muscle, and discuss their involvement during myogenesis and various skeletal muscle conditions. This review also provides important considerations for the accurate measurement of mitophagy and interpretation of data in skeletal muscle.</span></span></p></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"143 ","pages":"Pages 54-65"},"PeriodicalIF":7.3,"publicationDate":"2023-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9193474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Brandon J. Richards, Mikhaela Slavin, Ashley N. Oliveira, Victoria C. Sanfrancesco, David A. Hood
{"title":"Mitochondrial protein import and UPRmt in skeletal muscle remodeling and adaptation","authors":"Brandon J. Richards, Mikhaela Slavin, Ashley N. Oliveira, Victoria C. Sanfrancesco, David A. Hood","doi":"10.1016/j.semcdb.2022.01.002","DOIUrl":"https://doi.org/10.1016/j.semcdb.2022.01.002","url":null,"abstract":"<div><p><span><span><span>The biogenesis of mitochondria requires the coordinated expression of the nuclear and the mitochondrial genomes. However, the vast majority of gene products within the organelle are encoded in the nucleus, synthesized in the cytosol, and imported into mitochondria via the protein import machinery, which permit the entry of proteins to expand the mitochondrial network. Once inside, proteins undergo a maturation and folding process brought about by </span>enzymes comprising the </span>unfolded protein response (UPR</span><sup>mt</sup>). Protein import and UPR<sup>mt</sup><span> activity must be synchronized and matched with mtDNA-encoded subunit synthesis for proper assembly of electron transport chain<span> complexes to avoid proteotoxicity. This review discusses the functions of the import and UPR</span></span><sup>mt</sup> systems in mammalian skeletal muscle, as well as how exercise alters the equilibrium of these pathways in a time-dependent manner, leading to a new steady state of mitochondrial content resulting in enhanced oxidative capacity and improved muscle health.</p></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"143 ","pages":"Pages 28-36"},"PeriodicalIF":7.3,"publicationDate":"2023-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49724594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Implications of mitochondrial fusion and fission in skeletal muscle mass and health","authors":"Vanina Romanello , Marco Sandri","doi":"10.1016/j.semcdb.2022.02.011","DOIUrl":"10.1016/j.semcdb.2022.02.011","url":null,"abstract":"<div><p><span>The continuous dynamic reshaping of mitochondria by fusion and fission events is critical to keep mitochondrial quality and function under control in response to changes in energy and stress. Maintaining a functional, highly interconnected mitochondrial reticulum ensures rapid energy production and distribution. Moreover, mitochondrial networks act as dynamic signaling hub to adapt to the metabolic demands imposed by contraction, energy expenditure, and general metabolism. However, excessive mitochondrial fusion<span> or fission results in the disruption of the skeletal muscle mitochondrial network integrity and activates a retrograde response from mitochondria to the nucleus, leading to muscle atrophy, weakness and influencing whole-body homeostasis. These actions are mediated via the secretion of mitochondrial-stress myokines such as </span></span>FGF21<span> and GDF15. Here we will summarize recent discoveries in the role of mitochondrial fusion and fission in the control of muscle mass and in regulating physiological homeostasis and disease progression.</span></p></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"143 ","pages":"Pages 46-53"},"PeriodicalIF":7.3,"publicationDate":"2023-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9307789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}