2016
DOI: 10.1016/j.ijcard.2016.06.223
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PARP inhibition and postinfarction myocardial remodeling

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Cited by 16 publications
(11 citation statements)
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“…Currently, PARylation and AIF translocation were significantly higher in the HF group and correlation to reduced cardiac function and the clinical appearance of chronic heart failure (CHF; Barany et al ., ). Moreover, oxidative stress causes DNA breaks producing the activation of nuclear PARP‐1 enzyme that leads to energy depletion and unfavourable modulation of different kinase cascades (Akt‐1/GSK‐3β, MAPKs and various PKC isoforms), and thus, it promotes the development of HF (Halmosi et al ., ). The identification of PAR‐binding proteins and their characterization may provide a novel opportunity to understand the PAR‐signalling mechanisms and to develop low MW inhibitors to prevent toxic manifestations of parthanatos.…”
Section: Mechanisms Of Programmed Cardiomyocyte Necrosismentioning
confidence: 97%
“…Currently, PARylation and AIF translocation were significantly higher in the HF group and correlation to reduced cardiac function and the clinical appearance of chronic heart failure (CHF; Barany et al ., ). Moreover, oxidative stress causes DNA breaks producing the activation of nuclear PARP‐1 enzyme that leads to energy depletion and unfavourable modulation of different kinase cascades (Akt‐1/GSK‐3β, MAPKs and various PKC isoforms), and thus, it promotes the development of HF (Halmosi et al ., ). The identification of PAR‐binding proteins and their characterization may provide a novel opportunity to understand the PAR‐signalling mechanisms and to develop low MW inhibitors to prevent toxic manifestations of parthanatos.…”
Section: Mechanisms Of Programmed Cardiomyocyte Necrosismentioning
confidence: 97%
“…This may be due to the more severe damage in the allogeneic recipients. PARP activation induces ATP depletion by promoting mitochondrial damage and then induces ROS production, elevates intracellular Ca 2+ and destabilizes the mitochondrial membrane system leading to mitochondrial permeability transition and cell death (30–32). A recent study found that PARP increases the expression of inflammatory mediators such as cytokines, inducible nitric oxide synthase and adhesion molecules (33).…”
Section: Discussionmentioning
confidence: 99%
“…PARP activation induces ATP depletion by promoting mitochondrial damage and then induces reactive oxygen species production, elevates intracellular Ca 2+ ,, and destabilizes the mitochondrial membrane system leading to mitochondrial permeability transition and cell death. [30][31][32] A recent study found that PARP increases the expression of inflammatory mediators such as cytokines, inducible NO synthase, and adhesion molecules. 33 In our study, we found that CD47mAb-treated recipients had significantly lower PARP expression compared with the IgG-treated control group.…”
Section: Discussionmentioning
confidence: 99%
“…Acute myocardial infarction is followed by reperfusion, due to either coronary thrombolytic therapy or surgical intervention [175]. However, the return of oxygen to a respiratory chain that has suffered hypoxic damages during the preceding ischemia results in a substantial perfusion injury characterised by massive ROS and RNS production, upregulated expression of inflammatory cytokines, and PARP activation [176]. Additionally, the oxidative and nitrosative stress leads to endothelial dysfunction, transendothelial migration of neutrophils, JNK and p38 MAPK activation, DNA fragmentation, and myocardial injury [174].…”
Section: Atherosclerosis and Myocardial Infarctionmentioning
confidence: 99%
“…PARP1 activation is sustained long after the coronary reperfusion in the necrotic zone and the penumbra, resulting in impeded systolic and diastolic function of the left ventricle, Ca 2+ overload, and eventual cardiomyocyte death [178]. PARP inhibition achieved either by pharmacological means or by genetic manipulation significantly diminished the said detrimental effects in various experimental models [133,173,174,176]. Hearts of PARP1-deficient mice were reported to resist ischemic myocardial depression as well as reperfusion injury [179].…”
Section: Atherosclerosis and Myocardial Infarctionmentioning
confidence: 99%