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A muscle cell is also known as a myocyte when referring to either a cardiac muscle cell (cardiomyocyte) or a smooth muscle cell, as these are both small cells. A skeletal muscle cell is long and threadlike with many nuclei and is called a muscle fiber. Muscle cells (including myocytes and muscle fibers) develop from embryonic precursor cells called myoblasts. Myoblasts fuse from multinucleated skeletal muscle cells known as syncytia in a process known as myogenesis. Skeletal muscle cells and cardiac muscle cells both contain myofibrils and sarcomeres and form a striated muscle tissue. Cardiac muscle cells form the cardiac muscle in the walls of the heart chambers, and have a single central nucleus. Cardiac muscle cells are joined to neighboring cells by intercalated discs, and when joined in a visible unit they are described as a cardiac muscle fiber. Smooth muscle cells control involuntary movements such as the peristalsis contractions in the esophagus and

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Skeletal muscles (commonly referred to as muscles) are organs of the vertebrate muscular system and typically are attached by tendons to bones of a skeleton. The muscle cells of ske

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Muscle contraction is the activation of tension-generating sites within muscle cells. In physiology, muscle contraction does not necessarily mean muscle shortening because muscle tension can be produc

Cardiac muscle

Cardiac muscle (also called heart muscle or myocardium) is one of three types of vertebrate muscle tissues, with the other two being skeletal muscle and smooth muscle. It is an involuntary, striated m

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Evidence for a neuromuscular circuit involving hypothalamic interleukin-6 in the control of skeletal muscle metabolism

Ludger Jan Elzuë Goeminne, Vera Monica Lemos Da Silva, Barbara Moreira Crisol, Eduardo Rochete Ropelle

Hypothalamic interleukin-6 (IL6) exerts a broad metabolic control. Here, we demonstrated that IL6 activates the ERK1/2 pathway in the ventromedial hypothalamus (VMH), stimulating AMPK/ACC signaling and fatty acid oxidation in mouse skeletal muscle. Bioinformatics analysis revealed that the hypothalamic IL6/ERK1/2 axis is closely associated with fatty acid oxidation– and mitochondrial-related genes in the skeletal muscle of isogenic BXD mouse strains and humans. We showed that the hypothalamic IL6/ERK1/2 pathway requires the α2-adrenergic pathway to modify fatty acid skeletal muscle metabolism. To address the physiological relevance of these findings, we demonstrated that this neuromuscular circuit is required to underpin AMPK/ACC signaling activation and fatty acid oxidation after exercise. Last, the selective down-regulation of IL6 receptor in VMH abolished the effects of exercise to sustain AMPK and ACC phosphorylation and fatty acid oxidation in the muscle after exercise. Together, these data demonstrated that the IL6/ERK axis in VMH controls fatty acid metabolism in the skeletal muscle.

2022

ANTXR2 as a novel player in skeletal muscle stem cells

Lucie Josepha Marie Bracq, Françoise Gisou van der Goot Grunberg

PERGAMON-ELSEVIER SCIENCE LTD2021

A Tead1-Apelin axis directs paracrine communication from myogenic to endothelial cells in skeletal muscle

Benjamin D. Cosgrove, Maria Deak, Bart Deplancke, Sonia Karaz, Umji Lee, Julie Marie Russeil

Apelin (Apln) is a myokine that regulates skeletal muscle plasticity and meta-bolism and declines during aging. Through a yeast one-hybrid transcription factor binding screen, we identified the TEA domain transcription factor 1 (Tead1) as a novel regulator of the Apln promoter. Single-cell analysis of regenerating muscle revealed that the apelin receptor (Aplnr) is enriched in endothelial cells, whereas Tead1 is enriched in myogenic cells. Knock-down of Tead1 stimulates Apln secretion from muscle cells in vitro and myofiber-specific overexpression of Tead1 suppresses Apln secretion in vivo. Apln secretion via Tead1 knock-down in muscle cells stimulates endothelial cell expansion via endothelial Aplnr. In vivo, Apln peptide supplementation enhances endothelial cell expansion while Tead1 muscle overexpression delays endothelial remodeling following muscle injury. Our work describes a novel paracrine crosstalk in which Apln secretion is controlled by Tead1 in myogenic cells and influences endothelial remodeling during muscle repair.

CELL PRESS2022