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Autophagy

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...

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Related Experiment Video

Updated: Dec 14, 2025

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke

Published on: January 3, 2025

Autophagy and Ischemic Stroke.

Yanlin Zhang¹, Yongjun Cao¹, Chunfeng Liu²

¹Department of Neurology, The Second Affiliated Hospital of Soochow University, Suzhou, China.

Advances in Experimental Medicine and Biology

|July 17, 2020

Summary

This summary is machine-generated.

Autophagy, a cellular process, is activated during ischemic stroke and contributes to brain injury. Understanding autophagy

Keywords:

Apoptosis Autophagy Ischemic stroke Necrosis Self-adaption

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Last Updated: Dec 14, 2025

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Assessing Phagocytic Clearance of Cell Death in Experimental Stroke by Ligatable Fluorescent Probes

Assessing Phagocytic Clearance of Cell Death in Experimental Stroke by Ligatable Fluorescent Probes

Published on: May 27, 2014

Area of Science:

Neuroscience
Cell Biology
Pathology

Background:

Ischemic stroke causes brain tissue damage due to interrupted blood supply.
Autophagy is activated in brain cells like neurons and glial cells during ischemic stroke.
Autophagy dysfunction contributes to the pathology of ischemic stroke.

Purpose of the Study:

To outline the induction of basal autophagy and its role in neurons during ischemic stroke.
To explore the interplay between autophagy, necrosis, and apoptosis in ischemic stroke.
To review the involvement of autophagy in cerebral ischemic conditioning.

Main Methods:

Review of existing literature on autophagy and ischemic stroke.
Analysis of cellular mechanisms involving autophagy, oxidative stress, ER stress, and mitochondrial dysfunction.
Examination of autophagy's role in preconditioning, periconditioning, and postconditioning.

Main Results:

Autophagy activation is a key feature of ischemic stroke pathology.
Autophagy interacts with other cellular stress pathways (oxidative, ER, mitochondrial) in stroke.
Autophagy plays a significant role in the protective mechanisms of cerebral ischemic conditioning.

Conclusions:

Autophagy is a critical cellular process implicated in ischemic stroke pathogenesis and progression.
Targeting autophagy may offer therapeutic strategies for managing ischemic stroke.
Further research into autophagy's complex role in cerebral ischemic conditioning is warranted.