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Cytoprotective Mechanisms and the Regulation of Mitochondrial Permeability Transition
Sponsored by APS Endocrinology and Metabolism Section
Hypoxia and Oxidative Stress Tracks

Activation of “stress pathways” causes cell death and suppression of these pathways, either via direct inhibition or by stimulation of “survival” pathways like the MAPK or the phosphatidylinositol 3-OH kinase (PI3-K)-Akt cascades, is cytoprotective. These pro-death and pro-survival pathways converge upon the mitochondria, where they regulate the mitochondrial permeability transition (MPT) pore, a critical mediator of cell death. Building upon this, this Symposium is designed to address how estrogen (E2) physically and/or functionally interacts with mitochondria to induce cytoprotection. Moreover, the Symposium is intended to reflect the likelihood that the protective mechanism(s) activated by E2 are multi-factorial. Specifically, the Symposium will address (1) the genomic role of estrogens and estrogen receptors in the regulation of mitochondrial respiratory chain biogenesis, (2) non-genomic activation of specific signal transduction pathways by E2 with consequential protection against mitochondrial dysfunction, (3) modulation of glycogen synthase kinase activity and its influence on cardioprotection and (4) current models for the molecular architecture of the MPT pore and its regulation. The goal of the Symposium is to both provide information and stimulate discussion as to how E2-stimulated non-genomic and genomic responses might directly or indirectly influence the MPT pore, thereby preventing mitochondrial dysfunction and cell death.