Inhibiting mitochondrial permeability transition pore opening: a new paradigm for myocardial preconditioning?

By D. Hausenloy, H. Maddock, G. Baxter, D. Yellon. Cardiovascular Research, 2002

644 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Interaction of Cardiovascular Risk Factors with Myocardial Ischemia/Reperfusion Injury, Preconditioning, and Postconditioning (2007, background): “…known substrates that may be distal effector mechanisms of cytoprotection including activation of NOS (Zhang et al., 2005), inhibition of mPTP (Hausenloy et al., 2002, 2005b), up-regulation of antiapoptotic members, inhibition of proapoptotic members of the BclII family (Uchiyama et al.,…”
Mitochondrial permeability transition pore opening during myocardial reperfusion--a target for cardioprotection. (2004, background): “Indirect evidence obtained using isolated cardiac myocytes and mitochondria has implicated the inhibition of the MPTP in both calciumand diazoxide-mediated preconditioning [32,35,75].”
Preconditioning the myocardium: from cellular physiology to clinical cardiology. (2003, background): “(137) describes a new paradigm for preconditioning in which opening the mitoKATP channel could act to prevent opening of the mitochondrial transition pore described below.”
Myocardial ischemia-reperfusion injury: a neglected therapeutic target. (2013, positive): “…known MPTP inhibitors (such as the immunosuppressant cyclosporin A) at the onset of myocardial reperfusion has been reported in experimental studies to reduce MI size by 40%–50% in small and large animal MI models (37–40) and protect human atrial trabeculae subjected to simulated IRI (41).”