Abstract
Hepatic ischemia-reperfusion injury is a major cause of post-operative hepatic dysfunction and liver failure after transplantation. Mitochondrial pathways can be either beneficial or detrimental to hepatic cell apoptosis during hepatic ischemia/reperfusion injury, depending on multiple factors. Hepatic ischemia/reperfusion injury may be induced by opened mitochondrial permeability transition pore, released apoptosis-related proteins, up-regulated B-cell lymphoma-2 gene family proteins, unbalanced mitochondrial dynamics, and endoplasmic reticulum stress, which are integral parts of mitochondrial pathways. In this review, we discuss the role of mitochondrial pathways in apoptosis that account for the most deleterious effect of hepatic ischemia/reperfusion injury.
Highlights
Apoptosis is a normal physiological process of highly regulated cell death that occurs in most multicellular organisms [1]
Mitochondria play a key role in the apoptotic signal transduction pathway during cell apoptosis, which is manifested as electron transfer rupture of the mitochondrial respiratory chain, reactive oxygen species (ROS) production, adenosine triphosphate (ATP) depletion, decreased mitochondrial membrane potential, mitochondrial permeability transition pore (MPTP) opening, and even loss of release of outer membrane proteins, leading to cell apoptosis [7]
The early characteristics of hepatic ischemia/reperfusion injury (IRI) are the occurrence of oxidative stress and the release of ROS, which directly lead to hepatocyte injury [53]
Summary
Apoptosis is a normal physiological process of highly regulated cell death that occurs in most multicellular organisms [1]. Irreversible intracellular genomic damage is caused by various stimuli including gamma-ray irradiation, endoplasmic reticulum stress, growth factor deprivation, and oxidative stress, which activates the intrinsic pathway, known as the mitochondrial pathway [5,6]. This pathway is responsible for mitochondrial electron transport chain breakage, reactive oxygen species (ROS) production, adenosine triphosphate (ATP) depletion, mitochondrial membrane potential (∆Ψm) decrease, and mitochondrial permeability transition pore (MPTP) opening, leading to cell apoptosis [7]. Mitochondria play a key role in the apoptotic signal transduction pathway during cell apoptosis, which is manifested as electron transfer rupture of the mitochondrial respiratory chain, ROS production, ATP depletion, decreased mitochondrial membrane potential, MPTP opening, and even loss of release of outer membrane proteins, leading to cell apoptosis [7]. This review mainly discusses the role of mitochondrial apoptosis pathway in hepatic ischemia-reperfusion in recent years
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
