Modification of Ischemia/Reperfusion-Induced Alterations in Subcellular Organelles by Ischemic Preconditioning.
Paramjit S TappiaAnureet Kaur ShahBram RamjiawanNaranjan S DhallaPublished in: International journal of molecular sciences (2022)
It is now well established that ischemia/reperfusion (I/R) injury is associated with the compromised recovery of cardiac contractile function. Such an adverse effect of I/R injury in the heart is attributed to the development of oxidative stress and intracellular Ca 2+ -overload, which are known to induce remodeling of subcellular organelles such as sarcolemma, sarcoplasmic reticulum, mitochondria and myofibrils. However, repeated episodes of brief periods of ischemia followed by reperfusion or ischemic preconditioning (IP) have been shown to improve cardiac function and exert cardioprotective actions against the adverse effects of prolonged I/R injury. This protective action of IP in attenuating myocardial damage and subcellular remodeling is likely to be due to marked reductions in the occurrence of oxidative stress and intracellular Ca 2+ -overload in cardiomyocytes. In addition, the beneficial actions of IP have been attributed to the depression of proteolytic activities and inflammatory levels of cytokines as well as the activation of the nuclear factor erythroid factor 2-mediated signal transduction pathway. Accordingly, this review is intended to describe some of the changes in subcellular organelles, which are induced in cardiomyocytes by I/R for the occurrence of oxidative stress and intracellular Ca 2+ -overload and highlight some of the mechanisms for explaining the cardioprotective effects of IP.
Keyphrases
- oxidative stress
- diabetic rats
- ischemia reperfusion injury
- cerebral ischemia
- high glucose
- nuclear factor
- reactive oxygen species
- dna damage
- risk assessment
- induced apoptosis
- left ventricular
- toll like receptor
- endothelial cells
- brain injury
- subarachnoid hemorrhage
- heart failure
- atrial fibrillation
- skeletal muscle
- acute myocardial infarction
- drug induced
- smooth muscle
- adverse drug
- blood brain barrier
- inflammatory response
- sleep quality