Literature DB >> 27940349

Autophagy as a regulator of cardiovascular redox homeostasis.

Ye Yan1, Toren Finkel2.   

Abstract

Autophagy is a highly regulated process involving the removal of damaged proteins and organelles from cells and tissues through a lysosomal-mediated pathway. Accumulating evidence suggests that autophagy is necessary to maintain redox homeostasis. Here, we explore the connection between autophagy and reactive oxygen species (ROS). In particular, we discuss how oxidant-dependent signaling can modulate autophagic flux and how autophagy can, in turn, modulate ROS levels. Finally, we discuss how a decline or disruption of autophagy might contribute to redox-dependent cardiovascular pathology and help fuel the age-dependent decline in cardiovascular function.
Copyright © 2016. Published by Elsevier Inc.

Entities:  

Keywords:  Autophagy; Cardiovascular disease; Mitophagy; ROS

Mesh:

Substances:

Year:  2016        PMID: 27940349      PMCID: PMC5462893          DOI: 10.1016/j.freeradbiomed.2016.12.003

Source DB:  PubMed          Journal:  Free Radic Biol Med        ISSN: 0891-5849            Impact factor:   7.376


  66 in total

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3.  Keap1 degradation by autophagy for the maintenance of redox homeostasis.

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5.  ULK1/2 Constitute a Bifurcate Node Controlling Glucose Metabolic Fluxes in Addition to Autophagy.

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Journal:  Nature       Date:  2014-06-04       Impact factor: 49.962

Review 7.  Mitochondrial redox status as a target for cardiovascular disease.

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Journal:  Curr Opin Pharmacol       Date:  2016-02-16       Impact factor: 5.547

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  27 in total

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Review 5.  Endothelial Autophagy in Coronary Microvascular Dysfunction and Cardiovascular Disease.

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Journal:  Cells       Date:  2022-06-30       Impact factor: 7.666

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Review 7.  Targeting mitochondrial dysfunction and oxidative stress in heart failure: Challenges and opportunities.

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Review 8.  Self-eating and Heart: The Emerging Roles of Autophagy in Calcific Aortic Valve Disease.

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9.  Enhanced autophagy in Becn1F121A/F121A knockin mice counteracts aging-related neural stem cell exhaustion and dysfunction.

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Review 10.  Inflammation, a significant player of Ataxia-Telangiectasia pathogenesis?

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