The major purpose of this book is to review the evidence supporting the concept that intrinsic cell survival programs can be activated by a variety of mildly noxious stimuli or pharmacologic agents to confer protection against the deleterious effects of ischemia/reperfusion (I/R). We begin with a discussion of the concept of hormesis (a term used most extensively in the toxicologic literature which refers to biphasic cellular responses that depend on concentration or intensity of a stimulus), review the seminal studies that led to the discovery of the cardioprotective effects of ischemic preconditioning, and outline its therapeutic potential (Chapter 1). This is followed by a summary of our current understanding of the mechanisms of I/R injury (Chapter 2), as this provides several points of intervention in limiting postischemic tissue injury that may be targeted by the adaptive programs invoked by conditioning stimuli. Chapters 3 and 4 focus on the mechanisms underlying ischemic pre-, post-, and remote conditioning, which establishes the mechanistic rationale for development of pharmacologic conditioning strategies that may mimic the remarkably powerful effects of ischemic conditioning (and are covered in Chapter 5). Lifestyle interventions, including exercise, caloric restriction, and consumption of alcoholic beverages and/or phytochemicals, that may induce hormetic responses will also be reviewed in this chapter. While the promise for conditioning as a therapeutic approach is enormous, there are obstacles to its practical application in patients, which are covered in Chapter 6. The final chapter (Chapter 7) examines the extension of our mechanistic understanding of the signaling pathways invoked by conditioning stimuli into the realm of gene therapy and to the preservation of stem cell viability in the harsh ischemic environment as natural translational outgrowths of preconditioning into therapeutics.
... activation of cell survival programs (–) Figure 1.2 Tissue reactions to ischemia/reperfusion (I/R) are bimodal, ... Long duration and intense ischemia results in cell damage that can cause infarction, with reperfusion usually ...
In sharp contrast, short periods of ischemia (< 5 min) followed by reperfusion (ischemic conditioning) activate cell survival programs that limit the magnitude of injury induced by subsequent exposure to prolonged I/R. and Vatner, 2005, ...
Ischemic preconditioning of small bowel mitigates the late phase of reperfusion injury: heme oxygenase mediates cytoprotection. ... Cell survival programs and ischemia/reperfusion: hormesis, preconditioning, and cardioprotection.
This book focuses on the role of cardioprotection in surgery and the use of pharmacological therapies such as ACE-inhibitors, statins and beta-blockers in order to reduce the myocardial injury sustained by the patient and the significant ...
Cell survival programs and ischemia/reperfusion: Hormesis, preconditioning, and cardioprotection. In D. N. Granger & J. Granger (Eds.), Colloquium series on integrated systems physiology: From molecule to function to disease.
The Science of Hormesis in Health and Longevity provides a comprehensive review of mild stress-induced physiological hormesis and its role in the maintenance and promotion of health.
Arber S, Hunter JJ, Ross J Jr. et al. MLP-deficient mice exhibit a disruption of cardiac cytoarchitectural organization, dilated cardiomyopathy, and heart failure. Cell 1997; 88:393– 403. 4. Mohapatra B, Jimenez S, ...
Textbook of Gastrointestinal Radiology, 2nd ed. Philadelphia: WB Saunders; 2000: 627. Levine M.S., Ramchandani P., Rubesin S.E. Practical Fluoroscopy of the GI and GU Tracts. New York: Cambridge University Press; 2012.
The book explores how cardiac hormones are changed in various cardiac pathologies and the recent success that has been uncovered in their therapeutic use.
“Cell survival programs and ischemia/reperfusion: hormesis, preconditioning, and cardioprotection,” in Colloquium Series on Integrated Systems Physiology: From Molecule to Function to Disease, Vol. 109, eds D. N. Granger and J. Granger ...