Apoptosis: Pathophysiology and therapeutic implications for the cardiac surgeon

Khoynezhad, Ali; Jalali, Ziba; Tortólani, Anthony J.

doi:10.1016/j.athoracsur.2003.06.034

Cited by 33 publications

(25 citation statements)

References 73 publications

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“…(Ascione, et al, 2000;Caputo, et al, 2002;Nesher, et al, 2006)). CPB can impact upon the cellular and non-cellular elements of blood resulting in the activation of different pro-inflammatory cascades (Anselmi, et al, 2004;Hill, 1998;Khoynezhad, Jalali, & Tortolani, 2004;Rinder, 2006;Suleiman, Zacharowski, & Angelini, 2008). It is now generally accepted that CPB is a direct trigger of cardiac injury since miniaturized cardiopulmonary bypass is associated with less cardiac injury compared to conventional bypass (El-Essawi, et al, 2010;Nguyen, et al, 2014;Remadi, Rakotoarivelo, Marticho, & Benamar, 2006;Skrabal, Steinhoff, & Liebold, 2007).…”

Section: Systemic Inflammatory Response During Surgerymentioning

confidence: 98%

Inflammation, oxidative stress and postoperative atrial fibrillation in cardiac surgery

Zakkar

Ascione

James

et al. 2015

Pharmacology & Therapeutics

191

129

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Postoperative atrial fibrillation (POAF) is a common complication of cardiac surgery that occurs in up to 60% of patients. POAF is associated with increased risk of cardiovascular mortality, stroke and other arrhythmias that can impact on early and long term clinical outcomes and health economics. Many factors such as disease-induced cardiac remodelling, operative trauma, changes in atrial pressure and chemical stimulation and reflex sympathetic/parasympathetic activation have been implicated in the development of POAF. There is mounting evidence to support a major role for inflammation and oxidative stress in the pathogenesis of POAF. Both are consequences of using cardiopulmonary bypass and reperfusion following ischaemic cardioplegic arrest. Subsequently, several anti-inflammatory and antioxidant drugs have been tested in an attempt to reduce the incidence of POAF. However, prevention remains suboptimal and thus far none of the tested drugs has provided sufficient efficacy to be widely introduced in clinical practice. A better understanding of the cellular and molecular mechanisms responsible for the onset and persistence of POAF is needed to develop more effective prediction and interventions.

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Section: Systemic Inflammatory Response During Surgerymentioning

confidence: 98%

Inflammation, oxidative stress and postoperative atrial fibrillation in cardiac surgery

Zakkar

Ascione

James

et al. 2015

Pharmacology & Therapeutics

191

129

View full text Add to dashboard Cite

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“…The accelerated cell death is multifactorial and is influenced by host inflammatory response mediators, mechanical injury, maladaptation, bouts of ischemia and ischemia-reperfusion, and the origin and quality of the donor cell preparation [40]. However, apoptosis has been implicated as the main contributor in massive loss of donor cells [13,51]. Apoptosis, a highly orchestrated mechanism of programmed cell death, is initiated by both intrinsic and extrinsic factors.…”

Section: Acute-phase Cell Death and Approaches To Enhance Donor Cell mentioning

confidence: 98%

Preconditioning and Stem Cell Survival

Haider

Ashraf

2009

J. of Cardiovasc. Trans. Res.

111

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The harsh ischemic and cytokine-rich microenvironment in the infarcted myocardium, infiltrated by the inflammatory and immune cells, offers a significant challenge to the transplanted donor stem cells. Massive cell death occurs during transplantation as well as following engraftment which significantly lowers the effectiveness of the heart cell therapy. Various approaches have been adopted to overcome this problem nevertheless with multiple limitations with each of these current approaches. Cellular preconditioning and reprogramming by physical, chemical, genetic, and pharmacological manipulation of the cells has shown promise and "prime" the cells to the "state of readiness" to withstand the rigors of lethal ischemia in vitro as well as posttransplantation. This review summarizes the past and present novel approaches of ischemic preconditioning, pharmacological and genetic manipulation using preconditioning mimetics, recombinant growth factor protein treatment, and reprogramming of stem cells to overexpress survival signaling molecules, microRNAs, and trophic factors for intracrine, autocrine, and paracrine effects on cytoprotection.

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“…Myocardial cells provide multisignaling pathways in cell regulation. These multiple protein regulations contain phosphatidylinositol 3-kinase (PI3K), Akt, protein kinase B (PKB), and calcium ions (Catalucci and Condorelli 2006;Khoynezhad et al 2004;Lai et al 2003;Latronico et al 2004). Animal experiments have confirmed that IGF1 in the heart increases anti-apoptotic protein (Bcl-xL) mitochondrial performance in vivo (Yamamura et al 2001).…”

Section: Introductionmentioning

confidence: 99%

Exercise training enhanced SIRT1 longevity signaling replaces the IGF1 survival pathway to attenuate aging-induced rat heart apoptosis

Lai

Kuo³

et al. 2014

AGE

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Cardiovascular disease is the second leading cause of death (9.1 %) in Taiwan. Heart function deteriorates with age at a rate of 1 % per year. As society ages, we must study the serious problem of cardiovascular disease. SIRT1 regulates important cellular processes, including anti-apoptosis, neuronal protection, cellular senescence, aging, and longevity. In our previous studies, rats with obesity, high blood pressure, and diabetes exhibiting slowed myocardial performance and induced cell apoptosis were reversed via sports training AGE (2014) 36:9706

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Apoptosis: Pathophysiology and therapeutic implications for the cardiac surgeon

Cited by 33 publications

References 73 publications

Inflammation, oxidative stress and postoperative atrial fibrillation in cardiac surgery

Inflammation, oxidative stress and postoperative atrial fibrillation in cardiac surgery

Preconditioning and Stem Cell Survival

Exercise training enhanced SIRT1 longevity signaling replaces the IGF1 survival pathway to attenuate aging-induced rat heart apoptosis

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