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SESN2/sestrin2 suppresses sepsis by inducing mitophagy and inhibiting NLRP3 activation in macrophages

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TLDR
It is demonstrated that SESN2 (sestrin 2), known as stress-inducible protein, suppresses prolonged NLRP3 inflammasome activation by clearance of damaged mitochondria through inducing mitophagy in macrophages, defining a unique regulatory mechanism of mitophagic activation for immunological homeostasis that protects the host from sepsis.
Abstract
Proper regulation of mitophagy for mitochondrial homeostasis is important in various inflammatory diseases. However, the precise mechanisms by which mitophagy is activated to regulate inflammatory ...

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Status of Research on Sestrin2 and Prospects for its Application in Therapeutic Strategies Targeting Myocardial Aging.

TL;DR: In this paper , Sestrin2 has antioxidant and anti-inflammatory effects, stimulates autophagy, delays aging, regulates mitochondrial function, and inhibits myocardial remodeling by regulation of relevant signaling pathways.
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Progress in the mechanism of mitochondrial dysfunction in septic cardiomyopathy

TL;DR: In this article , a review of the mechanisms associated with mitochondrial dysfunction in septic cardiomyopathy and the mechanisms involved in order to find new insights into the study of septic cell disease was presented.
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Targeting the p53 signaling pathway in cancers: Molecular mechanisms and clinical studies

TL;DR: TriAP1 as mentioned in this paper is a novel p53 downstream inhibitor of apoptosis, which is the homolog of yeast mitochondrial intermembrane protein MDM35 and can play a tumor-promoting role by blocking the mitochondriadependent apoptosis pathway.
References
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Journal ArticleDOI

AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1

TL;DR: A molecular mechanism for regulation of the mammalian autophagy-initiating kinase Ulk1, a homologue of yeast ATG1, is demonstrated and a signalling mechanism for UlK1 regulation and autophagic induction in response to nutrient signalling is revealed.
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Methods in Mammalian Autophagy Research

TL;DR: Methods to monitor autophagy and to modulate autophagic activity are discussed, with a primary focus on mammalian macroautophagy.
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A role for mitochondria in NLRP3 inflammasome activation

TL;DR: It is shown that mitophagy/autophagy blockade leads to the accumulation of damaged, ROS-generating mitochondria, and this in turn activates the NLRP3 inflammasome, and may explain the frequent association of mitochondrial damage with inflammatory diseases.
Journal ArticleDOI

Parkin is recruited selectively to impaired mitochondria and promotes their autophagy

TL;DR: It is shown that Parkin is selectively recruited to dysfunctional mitochondria with low membrane potential in mammalian cells and this recruitment promotes autophagy of damaged mitochondria and implicate a failure to eliminate dysfunctional mitochondira in the pathogenesis of Parkinson's disease.
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Mechanisms of mitophagy

TL;DR: Mitophagy, the specific autophagic elimination of mitochondria, has been identified in yeast, and in mammals during red blood cell differentiation, mediated by NIP3-like protein X (NIX; also known as BNIP3L).
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