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<b>A. Regulation of Oxidative Stress</b><div><br><div>1.&nbsp;Impact of genetic and epigenetic factors on the oxidative stress in cardiovascular</div><div>disease</div><div><br></div><div>2.&nbsp;Role of aging and metabolic disease in oxidative stress of heart</div><div><br></div><div>3.&nbsp;Role of monoamine oxidases in heart diseases</div><div><br></div><div>4.&nbsp;Role of miRNA in oxidative stress induced heart diseases</div><div><br></div><div>5.&nbsp;Modulation of Oxidative (stressed) Heart Disease by Uncoupling Proteins</div><div><br></div>6.&nbsp;Redox regulation in heart by ion channels</div><div><br></div><div>7.&nbsp;Molecular regulators in ROS mediated cardiac diseases.</div><div><br></div><div>8.&nbsp;The inflammatory stress that follows preceded oxidative stresses in the pathogenesis</div><div>of heart diseases</div><div><br></div><div>9.&nbsp;Metabolic signatures of redox-dependent cardiovascular disease.</div><div><br></div><div>10.&nbsp;Role of heat shock proteins in oxidative stress induced heart diseases.</div><div><br></div><div><b>B. Pathophysiology of Oxidative Stress</b></div><div><br></div><div>11. Oxidative stress in metabolic syndrome : experimental model of biomarkers</div><div><br></div><div>12.&nbsp;Oxidative stress as a critical determinant of adult cardiac progenitor cell-fate</div><div>decisions</div><div><br></div><div>13.&nbsp;Role of oxidative stress in hyperhomocysteinemia-induced heart disease</div><div><br></div>14.&nbsp;Oxidative Stress and the Aging Heart<div><br></div><div>15.&nbsp;Basic mechanisms of ischemia/reperfusion injury leading to cellular and tissue</div><div>damage</div><div><br></div><div>16.&nbsp;Oxidative stress in congenital heart defects.</div><div><br></div><div>17.&nbsp;Nitrosative stress and cardiogenesis: Cardiac remodeling perturbs embryonic</div><div>metabolome</div><div><br></div><div>18.&nbsp;Oxidative Stress and Mitochondrial Dysfunction in Heart Diseases</div><div><br></div><div>19.&nbsp;Role of oxidative stress, mitochondrial dysfunction and autophagy in cardiovascular</div><div>disease: Its pathogenesis and amelioration by different small natural molecules</div><div><br></div><div>20.&nbsp;Regulation of cardiac ion channels in stress related heart diseases</div><div><br></div><div>21.In silico perspectives of the mechanism of oxidative stress during the onset of heart</div><div>disease.</div><div><br></div><div>22.Biomarkers of oxidative stress and endothelial dysfunction in the elderly: oxidized</div><div>LDL versus LDL oxidizability</div><div><br></div><div><b>C. Prevention & therapeutics</b></div><div><br></div><div>23.&nbsp;Restoring nitroso-redox balance as a therapeutic for heart disease</div><div><br></div><div>24.&nbsp;Oxidative stress role in cardiovascular prevention and disease</div><div><br></div><div>25.&nbsp;Mitochondrial dynamics and mitophagy in heart: role in disease and interventional</div><div>opportunities</div><div><br></div><div>26.&nbsp;Role of exercise in prevention and treatment of heart diseases: focus on redox balance</div><div><br></div><div>27.&nbsp;Mitochondrial biology and its therapeutic use in cardiovascular disease</div><div><br></div><div>28.&nbsp;Oxidative stress-driven cardiotoxicity of cancer drugs.</div><div><br></div><div>29.&nbsp;&nbsp;Modifying redox signaling to enhance success of regenerative therapy in the heart.</div><div><br></div>

<p><b>Dr Sajal Chakraborti</b> is a Professor of Biochemistry at the University of Kalyani, West Bengal, India. He completed his PhD at Calcutta University, Kolkata, India and his DSc at the University of Kalyani. He also pursued postdoctoral research at Johns Hopkins University, Baltimore; University of Utah, Salt Lake City; and New York Medical College, New York as a Fulbright Fellow. He visited the University of Florida, Gainesville, Florida, where he conducted research on f beta-adrenergic receptor activation in heart disease.&nbsp; His research mainly deals with the role of vasoactive agents in regulating vascular tone under oxidant and calcium signaling phenomena. He has been engaged in biochemistry teaching and research for the past 40 years (email:&nbsp;saj_chakra@rediffmail.com).&nbsp;</p>

<p><b>Dr Naranjan S Dhalla</b> is a Distinguished Professor at the University of Manitoba, Winnipeg, Canada. His expertise includes the subcellular and molecular basis of heart function in health and disease. He has been engaged in multidisciplinary cardiology research and education for over 50 years. He is currently the Editor-in-chief of Molecular and Cellular Biochemistry (Springer)&nbsp;(email:&nbsp;NSDhalla@sbrc.ca).&nbsp;</p>

<p><b>Dr Madhu Dixit</b> is a National Chair Fellow of the Translational Health Science and Technology Institute, Faridabad, Haryana, India. She has contributed to the general area of biochemical pharmacology with a special interest in cardiovascular pharmacology and redox biology. Dr Dixit has been engaged in research, especially on drug discovery and development, for over 40 years&nbsp;(email:&nbsp;rmadhudikshit@gmail.com).</p>

<p><b>Dr Nirmal K Ganguly</b>, a distinguished biotechnologist and former Director General of the Indian Council of Medical Research (ICMR), is associated with Global Health Strategies, New Delhi, India. One important aspect of his research is the understanding of occupational, environmental and nutritional aspects of heart disease.&nbsp; In 2008 he was presented with the Padma Bhushan Award in the field of “Medicine” by the President of India&nbsp;(email:&nbsp;ganguly1nk@gmail.com).&nbsp;</p><br>

<p>This book highlights the multifaceted roles of Reactive Oxygen Species (ROS) in modulating normal cellular and molecular mechanisms during the development of different types of heart disease. Each chapter in the book deals with the role that altered redox homeostasis plays in the pathophysiology of heart disease. In addition, the book explains how reactive oxidant species interact with their targets and provides novel strategies for attenuating oxidative stress-induced types of heart disease.</p><p>The book not only covers ROS-induced response in heart disease at the cellular level, but also demonstrates that an imbalance of redox states has its roots in our genes, and explains the ways gene expression is regulated. In turn, it reviews potential sources of ROS, their pathological effects on the heart, and potential sites for therapeutic interventions.</p>

<p>Uses multidisciplinary approach to demonstrate dysregulation of cellular redox status in the manifestation of different types of heart diseases</p><p>Describes the second messenger properties of ROS to activate signalling pathways involving different types of kinases, phosphatases, transcription factors and ion channels</p><p>Discusses different targets for drug development in cardiovascular diseases</p>