A mechanistic role for cardiac myocyte apoptosis in heart failure.
By D. Wencker, M. Chandra, Khanh Nguyen, W. Miao, S. Garantziotis, S. Factor, J. Shirani, R. Armstrong, R. Kitsis. Journal of Clinical Investigation, 2003
779 citations recorded by the source corpus.
Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/772cab8307ba41bafb5cf3c88e6fe687efdc53d0
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In Cardiology and Cardiovascular Medicine
- Joseph A. Hill
- P. Scherer
- E. Dale Abel
- K. Weeks
- Bianca C. Bernardo
- J. McMullen
- Haiming Cao
- M. Blüher
In Molecular Biology
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Citations in the corpus
- Anthracyclines: Molecular Advances and Pharmacologic Developments in Antitumor Activity and Cardiotoxicity (2004, background): “Although very low levels of myocyte apoptosis may be sufficient to cause dilated cardiomyopathy in laboratory animals (Wencker et al., 2003), the short-term wave of apoptosis induced by DOX in the rat should be opposed to the fact that, in patients with heart failure, apoptosis becomes gradually…”
- Cardiac remodeling in obesity. (2008, background): “Accordingly, inhibiting caspases can both reduce the occurrence of heart failure or slow its progression after MI (45, 131, 374, 383, 384) as well as improve contractile function (45).”
- The Pleiotropic Actions of Adiponectin are Initiated via Receptor-Mediated Activation of Ceramidase Activity (2010, background): “but without the upstream activation of death receptor”
- The role of autophagy in cardiomyocytes in the basal state and in response to hemodynamic stress (2007, background): “The level of apoptosis observed, however, seems too low for this to be a primary cause of cardiomyopathy in autophagy-deficient, pressure-overloaded hearts, as even a 15-fold increase in apoptosis resulted in only slowly progressive heart failur”
- Pathological Ventricular Remodeling: Mechanisms: Part 1 of 2 (2013, background): “Suppression of apoptosis decreases adverse remodeling and subsequent progression to heart failure in models of ischemia/reperfusion,(61) myocardial infarction–induced heart failure,(62) and nonischemic cardiomyopathy.(63) However, optimal timing of therapy, targets for inhibition within apoptotic si”
- Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets (2015, background): “However, in a setting of heart disease, the rate of cardiomyocyte apoptosis can increase in the human heart (Hein et al. 2003; Narula et al. 1996; Olivetti et al. 1997) and based on animal studies contributes to decompensated hypertrophy and HF (Hayakawa et al. 2003; Wencker et al. 2003).”
- Cardiac autophagy is a maladaptive response to hemodynamic stress. (2007, background): “Further, apoptosis has been implicated in the overall process of myocardial remodeling and the transition from cardiac hypertrophy to failure (23–25) although its relevance in acute and chronic heart disease is the subject of debate (26).”