Mitochondrial dysfunction plays a key role in the abrogation of cardioprotection by sodium hydrosulfide post-conditioning in diabetic cardiomyopathy rat heart

[1]  Peng Ye,et al.  Exogenous hydrogen sulfide attenuates the development of diabetic cardiomyopathy via the FoxO1 pathway , 2018, Journal of cellular physiology.

[2]  A. Mahalakshmi,et al.  Evaluating the impact of diabetes and diabetic cardiomyopathy rat heart on the outcome of ischemia‐reperfusion associated oxidative stress , 2018, Free radical biology & medicine.

[3]  J. Asara,et al.  Hypothalamic-Pituitary Axis Regulates Hydrogen Sulfide Production , 2017, Cell metabolism.

[4]  A. Papapetropoulos,et al.  Cardioprotection by H2S Donors: Nitric Oxide-Dependent and ‑Independent Mechanisms , 2016, The Journal of Pharmacology and Experimental Therapeutics.

[5]  G. Kurian,et al.  Hydrogen sulfide modulates sub-cellular susceptibility to oxidative stress induced by myocardial ischemic reperfusion injury. , 2016, Chemico-biological interactions.

[6]  S. Ravindran,et al.  Hydrogen sulfide post-conditioning preserves interfibrillar mitochondria of rat heart during ischemia reperfusion injury , 2016, Cell Stress and Chaperones.

[7]  D. Sanoudou,et al.  Cardioprotection by H2S engages a cGMP-dependent protein kinase G/phospholamban pathway. , 2015, Cardiovascular research.

[8]  J. Calvert,et al.  Hydrogen sulfide provides cardioprotection against myocardial/ischemia reperfusion injury in the diabetic state through the activation of the RISK pathway , 2014, Medical gas research.

[9]  Xiaoping Zhou,et al.  Hydrogen Sulfide Alleviates Diabetic Nephropathy in a Streptozotocin-induced Diabetic Rat Model , 2014, The Journal of Biological Chemistry.

[10]  J. Hollander,et al.  Functional deficiencies of subsarcolemmal mitochondria in the type 2 diabetic human heart. , 2014, American journal of physiology. Heart and circulatory physiology.

[11]  J. Guan,et al.  Treatment with hydrogen sulfide alleviates streptozotocin‐induced diabetic retinopathy in rats , 2013, British journal of pharmacology.

[12]  J. Calvert,et al.  Hydrogen sulfide preconditions the db/db diabetic mouse heart against ischemia-reperfusion injury by activating Nrf2 signaling in an Erk-dependent manner. , 2013, American journal of physiology. Heart and circulatory physiology.

[13]  E. Berenshtein,et al.  Energy status determines the distinct biochemical and physiological behavior of interfibrillar and sub-sarcolemmal mitochondria. , 2012, Biochemical and biophysical research communications.

[14]  S. Yuda,et al.  Diabetic cardiomyopathy: pathophysiology and clinical features , 2012, Heart Failure Reviews.

[15]  Ann E. Frazier,et al.  Biochemical analyses of the electron transport chain complexes by spectrophotometry. , 2012, Methods in molecular biology.

[16]  P. Schrauwen,et al.  Lipotoxicity in type 2 diabetic cardiomyopathy. , 2011, Cardiovascular research.

[17]  J. Duncan Mitochondrial dysfunction in diabetic cardiomyopathy. , 2011, Biochimica et biophysica acta.

[18]  N. Tentolouris,et al.  Diabetic cardiomyopathy: from the pathophysiology of the cardiac myocytes to current diagnosis and management strategies , 2010, Vascular health and risk management.

[19]  M. Powell,et al.  Mitochondrial dysfunction in the type 2 diabetic heart is associated with alterations in spatially distinct mitochondrial proteomes. , 2010, American journal of physiology. Heart and circulatory physiology.

[20]  S. Jha,et al.  Hydrogen Sulfide Mediates Cardioprotection Through Nrf2 Signaling , 2009, Circulation research.

[21]  R. Gibbons,et al.  Infarct size, ejection fraction, and mortality in diabetic patients with acute myocardial infarction treated with thrombolytic therapy. , 2007, American heart journal.

[22]  Csaba Szabo,et al.  Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function , 2007, Proceedings of the National Academy of Sciences.

[23]  R. Gibbons,et al.  Comparison of myocardial reperfusion in patients undergoing percutaneous coronary intervention in ST-segment elevation acute myocardial infarction with versus without diabetes mellitus (from the EMERALD Trial). , 2007, The American journal of cardiology.

[24]  E. Murphy,et al.  Primary and secondary signaling pathways in early preconditioning that converge on the mitochondria to produce cardioprotection. , 2004, Circulation research.

[25]  A. Baracca,et al.  Rhodamine 123 as a probe of mitochondrial membrane potential: evaluation of proton flux through F(0) during ATP synthesis. , 2003, Biochimica et biophysica acta.

[26]  G. Fiskum,et al.  Cyclosporin A-insensitive Permeability Transition in Brain Mitochondria , 2003, Journal of Biological Chemistry.

[27]  V. Skulachev,et al.  Mitochondrial filaments and clusters as intracellular power-transmitting cables. , 2001, Trends in biochemical sciences.

[28]  I. G. Fantus,et al.  Hyperglycemia-induced mitochondrial superoxide overproduction activates the hexosamine pathway and induces plasminogen activator inhibitor-1 expression by increasing Sp1 glycosylation. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[29]  D. Levy,et al.  Echocardiographic evidence for the existence of a distinct diabetic cardiomyopathy (the Framingham Heart Study). , 1991, The American journal of cardiology.

[30]  C. Hoppel,et al.  Biochemical properties of subsarcolemmal and interfibrillar mitochondria isolated from rat cardiac muscle. , 1977, The Journal of biological chemistry.

[31]  A. Grishman,et al.  New type of cardiomyopathy associated with diabetic glomerulosclerosis. , 1972, The American journal of cardiology.