Eric N. Churchill

TL;DR: Using an unbiased proteomic search, mitochondrial aldehyde dehydrogenase 2 (ALDH2) is identified as an enzyme whose activation correlates with reduced ischemic heart damage in rodent models and pharmacologic enhancement of ALDH2 activity may be useful for patients with wild-type or mutant AL DH2 who are subjected to cardiac ischemia.

TL;DR: It is demonstrated that PKCdelta activity and mitochondrial translocation at the onset of reperfusion mediates apoptosis by facilitating the accumulation and dephosphorylation of the pro-apoptotic BAD, cytochrome c release, PARP cleavage, and DNA laddering.

TL;DR: Progress has been made in establishing cytoprotective mechanisms, which arise as a consequence of epsilonPKC activation or deltaPKC inhibition, and how they may lead to protection in the setting of myocardial ischemia reperfusion, and the next challenge is to outline the molecular mechanisms regulated by delta and epsilusPKC isozymes that result in enhanced tolerance to IR.

TL;DR: The role of epsilonPKC in cardiac protection and on the signal transduction cascades that have been implicated in this protection are focused on.

TL;DR: The validity of therapeutically targeting PKC, an intracellular signaling enzyme, is discussed, and principles of pharmacology as they pertain to regulators of signaling cascades associated with these diseases are examined.