Autophagy, apoptosis, and cellular homeostasis: A physiological perspective
Keywords:
Autophagy, apoptosis, cellular homeostasis, cell signaling, physiology, programmed cell deathAbstract
Cellular homeostasis is a basic mechanism that keeps biological processes stable by balancing cell death and survival. The two main, interrelated processes that control this dynamic are autophagy and apoptosis. While apoptosis serves as a planned removal strategy for cells suffering irreversible damage, autophagy promotes stress adaption by preserving the quality of intracellular components. This review aims to analyze the functional relationship between autophagy, apoptosis, and cellular homeostasis from a physiological perspective, emphasizing the molecular mechanisms underlying the interaction of these two processes. Based on a synthesis of the most recent scientific literature from significant biomedical databases, this article is organized using a narrative review methodology. The findings demonstrate that autophagy and apoptosis are connected by a complex regulatory network that includes the mTOR, AMPK, p53, and Bcl-2 protein family pathways. Depending on the degree and duration of stress, this crosstalk enables cells to transition between executive and adaptive systems. Additionally, through controlling energy, ROS, and the release of pro-apoptotic substances, mitochondria serve as signal integration hubs that dictate the course of cellular reactions. One important factor in preserving cellular homeostasis is the ratio of autophagy to apoptosis. This system's dysregulation plays a major role in the pathophysiology of many illnesses, such as cancer and neurological conditions. The development of therapeutic approaches based on precise manipulation of cellular pathways is anticipated to be aided by a deeper comprehension of these integrative mechanisms.
Downloads
Published
How to Cite
Issue
Section
License
Copyright (c) 2026 Journal of Advanced Veterinary Research

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
Users have the right to read, download, copy, distribute, print, search, or link to the full texts of articles under the following conditions: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0).
Attribution-NonCommercial-NoDerivs
CC BY-NC-ND
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) license