Journal ArticleDOI
Cell Death in the Pathogenesis of Heart Disease: Mechanisms and Significance
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TLDR
Pharmacological and genetic inhibition of apoptosis and necrosis lessens infarct size and improves cardiac function in these disorders and a better understanding of these processes and their interrelationships may allow for the development of novel therapies for the major heart syndromes.Abstract:
Cell death was once viewed as unregulated. It is now clear that at least a portion of cell death is a regulated cell suicide process. This type of death can exhibit multiple morphologies. One of these, apoptosis, has long been recognized to be actively mediated, and many of its underlying mechanisms have been elucidated. Moreover, necrosis, the traditional example of unregulated cell death, is also regulated in some instances. Autophagy is usually a survival mechanism but can occur in association with cell death. Little is known, however, about how autophagic cells die. Apoptosis, necrosis, and autophagy occur in cardiac myocytes during myocardial infarction, ischemia/reperfusion, and heart failure. Pharmacological and genetic inhibition of apoptosis and necrosis lessens infarct size and improves cardiac function in these disorders. The roles of autophagy in ischemia/reperfusion and heart failure are unresolved. A better understanding of these processes and their interrelationships may allow for the development of novel therapies for the major heart syndromes.read more
Citations
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Journal ArticleDOI
Narrow time window of metabolic changes associated with transition to overt heart failure in Tgaq*44 mice
Elżbieta Czarnowska,Joanna Bierła,Marta Toczek,Urszula Tyrankiewicz,Urszula Tyrankiewicz,Beata Pająk,Beata Pająk,Dorota Domal-Kwiatkowska,Anna Ratajska,Ryszard T. Smolenski,Ulrike Mende,Stefan Chlopicki,Stefan Chlopicki +12 more
TL;DR: Three distinct phases of metabolic/structural changes during hypertrophy and progression to HF, with relatively short period of increase in FA metabolism, are highlighted, highlighting a narrow metabolic changes associated with transition to overt heart failure in Tgaq*44 mice that have therapeutic significance.
Journal ArticleDOI
A nucleus-targeted alternately spliced Nix/Bnip3L protein isoform modifies nuclear factor κB (NFκB)-mediated cardiac transcription
TL;DR: TNFα-stimulated cytoplasmic-nuclear shuttling of the alternately spliced non-mitochondrial Nix isoform is revealed and a role for sNix as a modulator of TNFα/NFκB- Stimulated cardiac gene expression is uncovered.
Book ChapterDOI
Molecular and Cellular Mechanisms in Heart Failure
Ilaria Puggia,Ilaria Puggia,Teisha J. Rowland,Shelley D. Miyamoto,Gianfranco Sinagra,Luisa Mestroni +5 more
TL;DR: Prognostic stratification and clinical management could benefit from identification of biomarkers such as inflammatory mediators or microRNA (miRNA), and miRNA and myocardial regenerative strategies are under investigations as potential novel therapeutic approaches.
Journal Article
Atractylodesin III maintains mitochondrial function and inhibits caspase-3 activity to reverse apoptosis of cardiomyocytes in AMI rats.
TL;DR: Atractylodesin III decreased apoptosis of myocardial cells in AMI, up-regulated Bcl-2 expression, and inhibited Bax and Caspase-3 activity.
References
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Journal ArticleDOI
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Journal ArticleDOI
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TL;DR: New insights into interactions among BCL-2 family proteins reveal how these proteins are regulated, but a unifying hypothesis for the mechanisms they use to activate caspases remains elusive.