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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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Sestrin2 Mediates IL-4-induced IgE Class Switching by Enhancing Germline ε Transcription in B Cells

TL;DR: In this paper, the role of Sesn2 in Ig class switching and Ig production in mouse B cells was investigated, and it was shown that the Sestrin2-AMPK signaling selectively enhances IL-4-induced GLTe expression and surface IgE (sIgE) expression in splenocytes.
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Pharmacological Progress of Mitophagy Regulation

TL;DR: A summary and status of the recently reported modulators of mitophagy can be found in this article , where the authors tried to summarize and summarize the most commonly used modulators.
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The Role of Mitochondrial Mutations in Chronification of Inflammation: Hypothesis and Overview of Own Data

TL;DR: This work proposes a hypothesis according to which mitochondrial DNA (mtDNA) mutations may play a key role in rendering certain cells prone to prolonged pro-inflammatory activation, therefore contributing to chronification of inflammation.
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Therapeutic effects of icariin and icariside II on diabetes mellitus and its complications.

TL;DR: In this paper , the authors present the general and toxicological information concerning icariin and icariside II and review the anti-DM effects from a molecular perspective, and discuss the potential benefits of icariins on the important pathological mechanisms of various diabetic complications, including diabetic cardiomyopathy, diabetic vascular endothelial disorder, diabetic nephropathy and diabetic erectile dysfunction.
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Activation of PINK1-mediated mitophagy protects bovine mammary epithelial cells against lipopolysaccharide-induced mitochondrial and inflammatory damage in vitro.

TL;DR: In this paper , the role of PINK1-mediated mitophagy on mitochondrial damage and inflammatory responses in bovine mammary epithelial cells challenged with lipopolysaccharide (LPS) was investigated.
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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