Calcium in Vascular Smooth Muscle Cell Elasticity and Adhesion: Novel Insights Into the Mechanism of Action

Zhu, Yi; Qu, Jing; He, Li; Zhang, Feng; Zhou, Zijing; Yang, Shanzhong; Zhou, Yong

doi:10.3389/fphys.2019.00852

Cited by 48 publications

(42 citation statements)

References 74 publications

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“…The regulation of Ca 2+ influx in muscle cells affects the contraction–relaxation cycle of muscle fibers, with significant consequences on the functions of many tissues, including blood vessels and bronchi [ 59 , 60 ]. Ca 2+ influx also affects muscle tissue development since it influences neuromuscular junction formation and their functionality through muscle nicotinic acetylcholine receptors (nAChRs) [ 61 ].…”

Section: The Role Of Mitochondria In Muscles and Physical Activitymentioning

confidence: 99%

Sport Performance and Manual Therapies: A Review on the Effects on Mitochondrial, Sarcoplasmatic and Ca2+ Flux Response

Regno¹,

Parisi

Chiera³

et al. 2021

Healthcare

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The present narrative review aims to highlight the possible effects manual therapies could have on cells and mitochondria, as these effects could improve athletic performance management. To this aim, this review summarizes the relationship between mechanical stimulation, with a special focus on physical activity, and cell response based on the most recent mechanobiology findings. Mechanobiology analyzes how cells respond to mechanical stressors coming from the environment. Indeed, endogenous (e.g., blood pressure, heartbeat and gastrointestinal motility) and exogenous (e.g., physical activity and manual therapies) stimuli can induce biochemical and epigenetic modifications that alter protein synthesis with heavy consequences on cell behavior. Mechanical stress can also influence mitochondrial behavior (i.e., biogenesis, autophagy, fusion, fission and energy production), sarcoplasmic response and calcium ion (Ca2+) flux. Since manual therapies have been shown to affect the extracellular matrix, which represents a primary source of mechanical stress that may alter both the cytoskeleton and mitochondrial metabolism, it is conceivable manual therapies could also affect cellular and mitochondrial behavior. Lastly, by suggesting possible directions for future laboratory and clinical studies, the authors expect this review to inspire further research on how manual therapies could affect bioenergetic metabolism and, thus, athletic performance.

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Section: The Role Of Mitochondria In Muscles and Physical Activitymentioning

confidence: 99%

Sport Performance and Manual Therapies: A Review on the Effects on Mitochondrial, Sarcoplasmatic and Ca2+ Flux Response

Regno¹,

Parisi

Chiera³

et al. 2021

Healthcare

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show abstract

“…Intracellular calcium is likely to regulate the mechanical properties of SMCs through a tight modulation of α5β1 integrin, α-SMA and cell-ECM interactions. The Ca 2+ dynamic across cells may activate the elasticity and the adhesion properties of vascular SMCs, with physiologically important consequences on vascular tone and resistance, and blood flow and pressure [53].…”

Section: Igf2r Modulates Vascular Remodeling and Skeletal Muscle Growthmentioning

confidence: 99%

Role of Insulin-Like Growth Factor Receptor 2 across Muscle Homeostasis: Implications for Treating Muscular Dystrophy

Torrente

Bella

Tripodi

et al. 2020

Cells

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The insulin-like growth factor 2 receptor (IGF2R) plays a major role in binding and regulating the circulating and tissue levels of the mitogenic peptide insulin-like growth factor 2 (IGF2). IGF2/IGF2R interaction influences cell growth, survival, and migration in normal tissue development, and the deregulation of IGF2R expression has been associated with growth-related disease and cancer. IGF2R overexpression has been implicated in heart and muscle disease progression. Recent research findings suggest novel approaches to target IGF2R action. This review highlights recent advances in the understanding of the IGF2R structure and pathways related to muscle homeostasis.

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“…In mice, vascular smooth muscle cell-specific PMCA1 knockout mice exhibit elevated blood pressure (Kobayashi et al, 2012). Mechanistically, loss of PMCA1 from vascular smooth muscle cells leads to enhanced expression of LTCC and increased Ca 2+ concentration which may affect smooth muscle cell stiffness and subsequently, vascular tone (Okuyama et al, 2018;Zhu et al, 2019). Furthermore, PMCA1 global heterozygous mice have increased hypertension with aging, which is preceded by vascular remodeling (Little et al, 2017).…”

Section: Pmcasmentioning

confidence: 99%

Targeting Ca2 + Handling Proteins for the Treatment of Heart Failure and Arrhythmias

2020

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Diseases of the heart, such as heart failure and cardiac arrhythmias, are a growing socioeconomic burden. Calcium (Ca 2+) dysregulation is key hallmark of the failing myocardium and has long been touted as a potential therapeutic target in the treatment of a variety of cardiovascular diseases (CVD). In the heart, Ca 2+ is essential for maintaining normal cardiac function through the generation of the cardiac action potential and its involvement in excitation contraction coupling. As such, the proteins which regulate Ca 2+ cycling and signaling play a vital role in maintaining Ca 2+ homeostasis. Changes to the expression levels and function of Ca 2+-channels, pumps and associated intracellular handling proteins contribute to altered Ca 2+ homeostasis in CVD. The remodeling of Ca 2+-handling proteins therefore results in impaired Ca 2+ cycling, Ca 2+ leak from the sarcoplasmic reticulum and reduced Ca 2+ clearance, all of which contributes to increased intracellular Ca 2+. Currently, approved treatments for targeting Ca 2+ handling dysfunction in CVD are focused on Ca 2+ channel blockers. However, whilst Ca 2+ channel blockers have been successful in the treatment of some arrhythmic disorders, they are not universally prescribed to heart failure patients owing to their ability to depress cardiac function. Despite the progress in CVD treatments, there remains a clear need for novel therapeutic approaches which are able to reverse pathophysiology associated with heart failure and arrhythmias. Given that heart failure and cardiac arrhythmias are closely associated with altered Ca 2+ homeostasis, this review will address the molecular changes to proteins associated with both Ca 2+handling and-signaling; their potential as novel therapeutic targets will be discussed in the context of pre-clinical and, where available, clinical data.

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Calcium in Vascular Smooth Muscle Cell Elasticity and Adhesion: Novel Insights Into the Mechanism of Action

Cited by 48 publications

References 74 publications

Sport Performance and Manual Therapies: A Review on the Effects on Mitochondrial, Sarcoplasmatic and Ca2+ Flux Response

Sport Performance and Manual Therapies: A Review on the Effects on Mitochondrial, Sarcoplasmatic and Ca2+ Flux Response

Role of Insulin-Like Growth Factor Receptor 2 across Muscle Homeostasis: Implications for Treating Muscular Dystrophy

Targeting Ca2 + Handling Proteins for the Treatment of Heart Failure and Arrhythmias

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