Plasma Fas Ligand, an Inducer of Apoptosis, and Plasma Soluble Fas, an Inhibitor of Apoptosis, in Patients With Chronic Congestive Heart Failure

Nishigaki, Kazuhiko; Minatoguchi, Shinya; Seishima, Mitsuru; Asano, Kiyoji; Noda, Toshiyuki; Yasuda, Norio; Sano, Hirotake; Kumada, Hirokazu; Takemura, Masao; Noma, Akio; Tanaka, Tsutomu; Watanabe, Soichi; Fujiwara, Hisayoshi

doi:10.1016/s0735-1097(97)00055-7

Cited by 151 publications

(69 citation statements)

References 32 publications

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“…Elevated levels of plasma-soluble Fas, but no increase in plasma-soluble Fas ligand, have been described in patients with congestive heart failure. 31 Although it is not known whether the myocardium expresses Fas ligand in vivo, it is possible that Fas-mediated apoptosis may be induced through Fas ligand present in the myocardium of patients with DCM.…”

Section: Discussionmentioning

confidence: 99%

Fas Expression and Apoptosis Correlate With Cardiac Dysfunction in Patients With Dilated Cardiomyopathy

et al. 1999

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Section: Discussionmentioning

confidence: 99%

Fas Expression and Apoptosis Correlate With Cardiac Dysfunction in Patients With Dilated Cardiomyopathy

et al. 1999

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“…Increased serum concentrations of proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) have been found in chronic heart failure (119). Another biomarker of chronic heart failure is the increased serum concentrations of Fas ligand (120). Both TNF-α and Fas ligand induce apoptosis of cardiomyocytes in various experimental studies (120,121).…”

Section: Cytokines and Other Factors In Myocardial Death Signalingmentioning

confidence: 99%

“…Another biomarker of chronic heart failure is the increased serum concentrations of Fas ligand (120). Both TNF-α and Fas ligand induce apoptosis of cardiomyocytes in various experimental studies (120,121). Other cytokines such as interleukin-6 are also found in the serum of patients with failing hearts (122)(123)(124).…”

Section: Cytokines and Other Factors In Myocardial Death Signalingmentioning

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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“…Plasma levels of the soluble forms of several members belonging to the tumour necrosis factor (TNF)-superfamily of apoptosis-related proteins (TNFa, TNF receptor (TNF-R) 1 and 2, Fas and Fas ligand) are increased in heart failure and correlate positively with New York Heart Association (NYHA) functional class [4,5]. Increased TNFrelated apoptosis-inducing ligand (TRAIL) cDNA expression is present in peripheral blood mononuclear cells of heart failure patients [6].…”

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confidence: 99%

Circulating apoptotic proteins are increased in long-term disease-free breast cancer survivors

et al. 2006

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Plasma Fas Ligand, an Inducer of Apoptosis, and Plasma Soluble Fas, an Inhibitor of Apoptosis, in Patients With Chronic Congestive Heart Failure

Abstract: We found elevated levels of plasma sFas and no increase in plasma sFas-L in human CHF. The increase in sFas may play an important role in the pathophysiologic mechanisms of CHF.

Cited by 151 publications

References 32 publications

Fas Expression and Apoptosis Correlate With Cardiac Dysfunction in Patients With Dilated Cardiomyopathy

Fas Expression and Apoptosis Correlate With Cardiac Dysfunction in Patients With Dilated Cardiomyopathy

Molecular and cellular mechanisms of cardiotoxicity.

Circulating apoptotic proteins are increased in long-term disease-free breast cancer survivors

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