Current Basic and Pathological Approaches to the Function of Muscle Cells and Tissues - From Molecules to Humans 2012
DOI: 10.5772/47772
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Cardiomyocyte and Heart Failure

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Cited by 3 publications
(2 citation statements)
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References 77 publications
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“…The main product of the RAAS is Ang-II, which has compensatory systemic effects that, if they persist, can exacerbate HF. This is because, in HF, Ang-II is stimulated to maintain cardiac output through increased vasoconstriction, salt retention, contractility, and the activation of inflammatory mediators [1,20,21]. The neuroendocrine pathological mechanisms of HF are regulated by the sympathetic nervous system and are linked to the RAAS [21].…”
Section: Discussionmentioning
confidence: 99%
“…The main product of the RAAS is Ang-II, which has compensatory systemic effects that, if they persist, can exacerbate HF. This is because, in HF, Ang-II is stimulated to maintain cardiac output through increased vasoconstriction, salt retention, contractility, and the activation of inflammatory mediators [1,20,21]. The neuroendocrine pathological mechanisms of HF are regulated by the sympathetic nervous system and are linked to the RAAS [21].…”
Section: Discussionmentioning
confidence: 99%
“…The number of cardiomyocytes usually decreases during HF (Nakano et al, 2012). Although the cause of this loss has not been fully clarified, it is known that cardiomyocytes are exposed to many different stressors in HF (Richardson et al, 1996;Chien, 1999).…”
Section: Regulation Of Ctgf In Response To Er Stressmentioning
confidence: 99%