2018
DOI: 10.1590/1678-4324-2017160244
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Apoptosis and Histopathology of the Heart after Renal Ischemia-Reperfusion in Male Rat Running title: Ischemia-Reperfusion Injury

Abstract: Ischemia-reperfusion injury was seen in strokes, myocardial infarctions, acute kidney injury, mesenteric ischemia

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Cited by 3 publications
(3 citation statements)
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“…It is reported that the renal ischemia reperfusion could dramatically decrease expression of Bcl-2 and increase expression of Bax in the brain tissue of I/R rats [54]. Although reports that male rats subjected 45 min of kidney ischemia indicate increasing connective tissue in the heart muscles myofibrils as a sign of tissue injury and apoptosis of myofibrils after 24 h reperfusion following kidney I/R [55]. Losing mitochondrial outer membrane could release cytochrome C and other mitochondrial proteins in cytosol which can activate apoptotic caspases such as the main executive protease: Caspase 3 [56].…”
Section: Discussionmentioning
confidence: 99%
“…It is reported that the renal ischemia reperfusion could dramatically decrease expression of Bcl-2 and increase expression of Bax in the brain tissue of I/R rats [54]. Although reports that male rats subjected 45 min of kidney ischemia indicate increasing connective tissue in the heart muscles myofibrils as a sign of tissue injury and apoptosis of myofibrils after 24 h reperfusion following kidney I/R [55]. Losing mitochondrial outer membrane could release cytochrome C and other mitochondrial proteins in cytosol which can activate apoptotic caspases such as the main executive protease: Caspase 3 [56].…”
Section: Discussionmentioning
confidence: 99%
“…Assessment is based on observations of 10 view fields with ×400 magnification. Histological changes scored on a 4-point scale: (−) none, (+) mild, (++) moderate, and (+++) severe damage [11]. The morphological measurement was…”
Section: Histopathological Assessmentmentioning
confidence: 99%
“…11 AKI-induced cardiac injury is mostly mediated by activation of the sympathetic nervous system (SNS) or unstable renin–angiotensin–aldosterone system (RAAS). 12 Cardiomyopathy and cell apoptosis are elevated in the heart tissue 24 h after IRI 13 and defective cardiac mitochondria may be important in heart injury of AKI patients. 14 Loss of memory and neural cell apoptosis along with blood-brain barrier (BBB) disruption were found during bilateral renal I/R as a result of kidney-brain crosstalk.…”
Section: Introductionmentioning
confidence: 99%