<abstract xmlns="http://www.w3.org/1999/xhtml"><p>Apoptosis is an inborn process that has been preserved during evolution; it allows the cells to systematically inactivate, destroy and dispose of their own components thus leading to their death. This program can be activated by both intra and extracellular mechanisms. The intracellular components involve a genetically defined development program while the extracellular aspects regard endogenous proteins, cytokines and hormones as well as xenobiotics, radiations, oxidative stress and hypoxia. The ability of a cell to enter apoptosis as a response to a „death” signal depends on its proliferative status, the position in the cell cycle and also on the controlled expression of those genes that have the capacity of promoting and inhibiting cell death. The fine regulation of these parameters needs to be maintained in order to ensure the physiological environment required for the induction of apoptosis.</p><p>In this review, we first describe evidence for the role of apoptotic pathways in ischemic acute renal failure, and then consider the potential mechanisms that may participate in this model of acute renal tubular injury. Potential therapeutic interventions to prevent tubular apoptosis in renal disease include angiotensin system inhibition, whereby the angiotensin II AT2 receptor blockade seems more promising in apoptosis inhibition than the inhibition of other receptor subtypes. A better understanding of the mechanisms of apoptosis could lead to safer and more specific therapeutic interventions for acute kidney injury.</p></abstract>

Apoptosis is an inborn process that has been preserved during evolution; it allows the cells to systematically inactivate, destroy and dispose of their own components thus leading to their death. This program can be activated by both intra and extracellular mechanisms. The intracellular components involve a genetically defined development program while the extracellular aspects regard endogenous proteins, cytokines and hormones as well as xenobiotics, radiations, oxidative stress and hypoxia. The ability of a cell to enter apoptosis as a response to a „death” signal depends on its proliferative status, the position in the cell cycle and also on the controlled expression of those genes that have the capacity of promoting and inhibiting cell death. The fine regulation of these parameters needs to be maintained in order to ensure the physiological environment required for the induction of apoptosis.In this review, we first describe evidence for the role of apoptotic pathways in ischemic acute renal failure, and then consider the potential mechanisms that may participate in this model of acute renal tubular injury. Potential therapeutic interventions to prevent tubular apoptosis in renal disease include angiotensin system inhibition, whereby the angiotensin II AT2 receptor blockade seems more promising in apoptosis inhibition than the inhibition of other receptor subtypes. A better understanding of the mechanisms of apoptosis could lead to safer and more specific therapeutic interventions for acute kidney injury.

Apoptosis in Acute Kidney Injury

“Carol Davila” University of Medicine and Pharmacy

Internal Medicine

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

{"article-title":"Apoptosis in Acute Kidney Injury"}

Apoptosis is an inborn process that has been preserved during evolution; it allows the cells to systematically inactivate, destroy and dispose of their own...

Apoptosis in Acute Kidney Injury

Publicado en línea: 12 mar 2020

Páginas: 45 - 53

DOI: https://doi.org/10.2478/inmed-2020-0101

Palabras clave
acute kidney injury, apoptosis, necrosis, ischaemia reperfusion, toxic renal injury

© 2020 Marilena Stoian et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Apoptosis in Acute Kidney Injury

Publicado en línea: 12 mar 2020

Páginas: 45 - 53

DOI: https://doi.org/10.2478/inmed-2020-0101

Palabras claveacute kidney injury, apoptosis, necrosis, ischaemia reperfusion, toxic renal injury

© 2020 Marilena Stoian et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Palabras clave
acute kidney injury, apoptosis, necrosis, ischaemia reperfusion, toxic renal injury