Shirin Doroudgar

Latest

• Proteomic analysis of the cardiac myocyte secretome reveals extracellular protective functions for the ER stress response.
• Mesencephalic astrocyte-derived neurotrophic factor is an ER-resident chaperone that protects against reductive stress in the heart.
• ATF6 Regulates Cardiac Hypertrophy by Transcriptional Induction of the mTORC1 Activator, Rheb.
• ATF6 Decreases Myocardial Ischemia/Reperfusion Damage and Links ER Stress and Oxidative Stress Signaling Pathways in the Heart.
• Junctophilin-2 gene therapy rescues heart failure by normalizing RyR2-mediated Ca(2+) release.
• S100A4 protects the myocardium against ischemic stress.
• Hrd1 and ER-Associated Protein Degradation, ERAD, are Critical Elements of the Adaptive ER Stress Response in Cardiac Myocytes.
• PRAS40 prevents development of diabetic cardiomyopathy and improves hepatic insulin sensitivity in obesity.
• Mechanistic target of rapamycin complex 2 protects the heart from ischemic damage.
• Pathological hypertrophy amelioration by PRAS40-mediated inhibition of mTORC1.
• Regulation of cardiac hypertrophic signaling by prolyl isomerase Pin1.
• New concepts of endoplasmic reticulum function in the heart: programmed to conserve.
• ATF6 [corrected] and thrombospondin 4: the dynamic duo of the adaptive endoplasmic reticulum stress response.
• Limitation of individual folding resources in the ER leads to outcomes distinct from the unfolded protein response.
• Mesencephalic astrocyte-derived neurotrophic factor protects the heart from ischemic damage and is selectively secreted upon sarco/endoplasmic reticulum calcium depletion.
• The cardiokine story unfolds: ischemic stress-induced protein secretion in the heart.
• Ischemia activates the ATF6 branch of the endoplasmic reticulum stress response.