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A Cathepsin D-Cleaved 16 kDa Form of Prolactin Mediates Postpartum Cardiomyopathy
Interaction of Cardiovascular Risk Factors with Myocardial Ischemia/Reperfusion Injury, Preconditioning, and Postconditioning
The aim of this review is to show the potential for developing cardioprotective drugs on the basis of endogenousCardioprotection by pre- and postconditioning and to review the evidence that comorbidities and aging accompanying coronary disease modify responses to ischemia/reperfusion and the cardiop Rotection conferred by preconditioning and post conditioning.
Inhibition of permeability transition pore opening by mitochondrial STAT3 and its role in myocardial ischemia/reperfusion
- K. Boengler, D. Hilfiker-Kleiner, G. Heusch, R. Schulz
- BiologyBasic Research in Cardiology
- 20 October 2010
The mitochondrial localization of STAT3 and its impact on respiration and MPTP opening was characterized and it was found that STAT3 was mainly present in the matrix of subsarcolemmal and interfibrillar cardiomyocyte mitochondria.
Interaction of Risk Factors, Comorbidities, and Comedications with Ischemia/Reperfusion Injury and Cardioprotection by Preconditioning, Postconditioning, and Remote Conditioning
- P. Ferdinandy, D. Hausenloy, G. Heusch, G. Baxter, R. Schulz
- Biology, MedicinePharmacological Reviews
- 1 October 2014
The critical need to take into account the presence of cardiovascular risk factors and concomitant medications when designing preclinical studies for the identification and validation of cardioprotective drug targets and clinical studies is emphasized.
Postconditioning and protection from reperfusion injury: where do we stand? Position paper from the Working Group of Cellular Biology of the Heart of the European Society of Cardiology.
Understanding of the underlying mechanisms must be improved to develop new therapeutic strategies to be applied at reperfusion with the ultimate aim of limiting the burden of ischaemic heart disease and potentially providing protection for other organs at risk of reperfusions injury, such as brain and kidney.
Nitric oxide in myocardial ischemia/reperfusion injury.
Cardioprotection: nitric oxide, protein kinases, and mitochondria.
The cumulative effect of stunning is a progression to hibernation, and repetitive cycles of ischemia/reperfusion with subsequent stunning finally result in hibernating myocardium with reduced contractile function and baseline blood flow.
High-Density Lipoproteins and Their Constituent, Sphingosine-1-Phosphate, Directly Protect the Heart Against Ischemia/Reperfusion Injury In Vivo via the S1P3 Lysophospholipid Receptor
The data demonstrate that HDL and its constituent, S1P, acutely protect the heart against ischemia/reperfusion injury in vivo via an S 1P3-mediated and NO-dependent pathway and a rapid therapeutic elevation of S1p-containing HDL plasma levels may be beneficial in patients at high risk of acute myocardial ischemIA.
Plasma nitrite reflects constitutive nitric oxide synthase activity in mammals.