Pathophysiology of heart failure and the renin-angiotensin-system

Holtz, J.

doi:10.1007/978-3-642-72497-8_13

Cited by 34 publications

(24 citation statements)

References 56 publications

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“…29 Angiotensin is an oligopeptide that causes vasoconstriction and increased blood pressure. Recent studies indicate that Ang II and TGF␤1 do not act independently from one another but act as part of an integrated signaling network that promotes cardiac remodeling and possibly fibrosis.…”

Section: Angiotensin IImentioning

confidence: 99%

Potential Therapeutic Targets for Cardiac Fibrosis

Leask

2010

Circulation Research

599

309

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Section: Angiotensin IImentioning

confidence: 99%

Potential Therapeutic Targets for Cardiac Fibrosis

Leask

2010

Circulation Research

599

309

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“…Further extensive studies are warranted for a comprehensive understanding of this field. (27,28). The compensatory response in turn activates counterregulatory mechanisms such as upregulation of atrial natriuretic peptide (ANP) expression (29,30).…”

Section: Myocardial Responses To Environmental Toxicantsmentioning

confidence: 99%

Molecular and cellular mechanisms of cardiotoxicity.

Kang

2001

Environ Health Perspect

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Cardiotoxicity resulting from detrimental environmental insults has been recognized for a long time. However, extensive studies of the mechanisms involved had not been undertaken until recent years. Advances in molecular biology provide powerful tools and make such studies possible. We are gathering information about cellular events, signaling pathways, and molecular mechanisms of myocardial toxicologic responses to environmental toxicants and pollutants. Severe acute toxic insults cause cardiac cell death instantly. In the early response to mild environmental stimuli, biochemical changes such as alterations in calcium homeostasis occur. These may lead to cardiac arrhythmia, which most often is reversible. Prolonged stimuli activate transcription factors such as activator protein-1 through elevation of intracellular calcium and the subsequent activation of calcineurin. Upregulation by activated transcription factors of hypertrophic genes results in heart hypertrophy, which is a short-term adaptive response to detrimental factors. However, further development of hypertrophy will lead to severe and irreversible cardiomyopathy, and eventually heart failure. From cardiac hypertrophy to heart failure, myocardial cells undergo extensive biochemical and molecular changes. Cardiac hypertrophy causes tissue hypoperfusion, which activates compensatory mechanisms such as production of angiotensin II and norepinephrine. Both further stimulate cardiac hypertrophy and, importantly, activate counterregulatory mechanisms including overexpression of atrial natriuretic peptide and b-type natriuretic peptide, and production of cytokines such as tumor necrosis factor-alpha. This counterregulation leads to myocardial remodeling as well as cell death through apoptosis and necrosis. Cell death through activation of mitochondrial factors and other pathways constitutes an important cellular mechanism of heart failure. Our current knowledge of cardiotoxicity is limited. Further extensive studies are warranted for a comprehensive understanding of this field.

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“…Angiotensin II (AngII) has been recognized as a potent hypertrophic and fibrotic stimulus elevated in the overloaded heart (Gray et al, 1998;Holtz, 1993;Leask, 2010). The adverse cardiac effects of AngII are mediated among others by endothelin-1 (ET-1) and transforming growth factor-β (TGFβ) (Herizi et al, 1998;Schultz et al, 2002;Gonzalez et al, 2004).…”

Section: Introductionmentioning

confidence: 99%