Limits...
The divergent roles of autophagy in ischemia and preconditioning.

Sheng R, Qin ZH - Acta Pharmacol. Sin. (2015)

Bottom Line: Autophagy is an evolutionarily conserved and lysosome-dependent process for degrading and recycling cellular constituents.Autophagy then interacts with apoptotic and necrotic signaling pathways to regulate cell death.Autophagy may also maintain cell function by removing protein aggregates or damaged mitochondria.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology and Laboratory of Aging and Nervous Diseases, Soochow University School of Pharmaceutical Science, Suzhou 215123, China.

ABSTRACT
Autophagy is an evolutionarily conserved and lysosome-dependent process for degrading and recycling cellular constituents. Autophagy is activated following an ischemic insult or preconditioning, but it may exert dual roles in cell death or survival during these two processes. Preconditioning or lethal ischemia may trigger autophagy via multiple signaling pathways involving endoplasmic reticulum (ER) stress, AMPK/TSC/mTOR, Beclin 1/BNIP3/SPK2, and FoxO/NF-κB transcription factors, etc. Autophagy then interacts with apoptotic and necrotic signaling pathways to regulate cell death. Autophagy may also maintain cell function by removing protein aggregates or damaged mitochondria. To date, the dual roles of autophagy in ischemia and preconditioning have not been fully clarified. The purpose of the present review is to summarize the recent progress in the mechanisms underlying autophagy activation during ischemia and preconditioning. A better understanding of the dual effects of autophagy in ischemia and preconditioning could help to develop new strategies for the preventive treatment of ischemia.

Show MeSH

Related in: MedlinePlus

A simplified scheme depicting some of the basic signaling pathways involved in the dual roles of autophagy during ischemia and preconditioning. The autophagy-lysosomal pathway may be activated by endoplasmic reticulum (ER) stress, AMPK/TSC1/2/mTOR, Beclin 1/BNIP3/SPK2 and FoxO and NF-κB transcription signaling. Mild autophagy may remove protein aggregation and damaged mitochondria or relieve excessive ER stress to prevent cell apoptosis or necrosis, whereas excessive autophagy may promote autophagic cell death or apoptosis via cathepsins.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4387298&req=5

fig1: A simplified scheme depicting some of the basic signaling pathways involved in the dual roles of autophagy during ischemia and preconditioning. The autophagy-lysosomal pathway may be activated by endoplasmic reticulum (ER) stress, AMPK/TSC1/2/mTOR, Beclin 1/BNIP3/SPK2 and FoxO and NF-κB transcription signaling. Mild autophagy may remove protein aggregation and damaged mitochondria or relieve excessive ER stress to prevent cell apoptosis or necrosis, whereas excessive autophagy may promote autophagic cell death or apoptosis via cathepsins.

Mentions: In summary, preconditioning or lethal ischemia may trigger autophagy via multiple signaling pathways involving ER stress, AMPK/TSC/mTOR, Beclin 1/BNIP3/SPK2, and transcription factors, etc (Figure 1). These signaling pathways may act together in a coordinated manner rather than independently and form a complex network to regulate autophagy activation. The relationship among the distinct signaling pathways involved in autophagy activation as well as the different roles of autophagy during ischemia and preconditioning remains a challenging research topic for future investigation.


The divergent roles of autophagy in ischemia and preconditioning.

Sheng R, Qin ZH - Acta Pharmacol. Sin. (2015)

A simplified scheme depicting some of the basic signaling pathways involved in the dual roles of autophagy during ischemia and preconditioning. The autophagy-lysosomal pathway may be activated by endoplasmic reticulum (ER) stress, AMPK/TSC1/2/mTOR, Beclin 1/BNIP3/SPK2 and FoxO and NF-κB transcription signaling. Mild autophagy may remove protein aggregation and damaged mitochondria or relieve excessive ER stress to prevent cell apoptosis or necrosis, whereas excessive autophagy may promote autophagic cell death or apoptosis via cathepsins.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4387298&req=5

fig1: A simplified scheme depicting some of the basic signaling pathways involved in the dual roles of autophagy during ischemia and preconditioning. The autophagy-lysosomal pathway may be activated by endoplasmic reticulum (ER) stress, AMPK/TSC1/2/mTOR, Beclin 1/BNIP3/SPK2 and FoxO and NF-κB transcription signaling. Mild autophagy may remove protein aggregation and damaged mitochondria or relieve excessive ER stress to prevent cell apoptosis or necrosis, whereas excessive autophagy may promote autophagic cell death or apoptosis via cathepsins.
Mentions: In summary, preconditioning or lethal ischemia may trigger autophagy via multiple signaling pathways involving ER stress, AMPK/TSC/mTOR, Beclin 1/BNIP3/SPK2, and transcription factors, etc (Figure 1). These signaling pathways may act together in a coordinated manner rather than independently and form a complex network to regulate autophagy activation. The relationship among the distinct signaling pathways involved in autophagy activation as well as the different roles of autophagy during ischemia and preconditioning remains a challenging research topic for future investigation.

Bottom Line: Autophagy is an evolutionarily conserved and lysosome-dependent process for degrading and recycling cellular constituents.Autophagy then interacts with apoptotic and necrotic signaling pathways to regulate cell death.Autophagy may also maintain cell function by removing protein aggregates or damaged mitochondria.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology and Laboratory of Aging and Nervous Diseases, Soochow University School of Pharmaceutical Science, Suzhou 215123, China.

ABSTRACT
Autophagy is an evolutionarily conserved and lysosome-dependent process for degrading and recycling cellular constituents. Autophagy is activated following an ischemic insult or preconditioning, but it may exert dual roles in cell death or survival during these two processes. Preconditioning or lethal ischemia may trigger autophagy via multiple signaling pathways involving endoplasmic reticulum (ER) stress, AMPK/TSC/mTOR, Beclin 1/BNIP3/SPK2, and FoxO/NF-κB transcription factors, etc. Autophagy then interacts with apoptotic and necrotic signaling pathways to regulate cell death. Autophagy may also maintain cell function by removing protein aggregates or damaged mitochondria. To date, the dual roles of autophagy in ischemia and preconditioning have not been fully clarified. The purpose of the present review is to summarize the recent progress in the mechanisms underlying autophagy activation during ischemia and preconditioning. A better understanding of the dual effects of autophagy in ischemia and preconditioning could help to develop new strategies for the preventive treatment of ischemia.

Show MeSH
Related in: MedlinePlus