Hypoxic postconditioning-induced neuroprotection increases neuronal autophagy via activation of the SIRT1/FoxO1 signaling pathway in rats with global cerebral ischemia

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Hypoxic postconditioning (HPC) has been reported to be a beneficial and promising treatment for global cerebral ischemia (GCI). However, its neuroprotective mechanism remains unclear. The aim of the present study was to determine whether the protective effects of HPC in a rat model of GCI were due to the upregulation of autophagy via the silent information regulator transcript-1 (SIRT1)/Forkhead box protein 1 (FoxO1) pathway. Morris water maze test revealed that HPC attenuated cognitive damage in GCI rats. HPC also significantly increased the levels of the autophagy-related protein LC3-II, SIRT1 and FoxO1 compared with those in the GCI group. However, the HPC-induced LC3-II upregulation was blocked by the SIRT1 inhibitor EX527. These results suggested that the beneficial effects of HPC on GCI rats were due to the upregulation of ischemiainduced autophagy and involved the SIRT1/FoxO1 signaling pathway.

Related collections

Most cited references 53

Record: found
Abstract: found
Article: not found

Autophagy: process and function.

Noboru Mizushima (2007)

Autophagy is an intracellular degradation system that delivers cytoplasmic constituents to the lysosome. Despite its simplicity, recent progress has demonstrated that autophagy plays a wide variety of physiological and pathophysiological roles, which are sometimes complex. Autophagy consists of several sequential steps--sequestration, transport to lysosomes, degradation, and utilization of degradation products--and each step may exert different function. In this review, the process of autophagy is summarized, and the role of autophagy is discussed in a process-based manner.

0 comments Cited 580 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Mitochondrial dysfunction and sarcopenia of aging: from signaling pathways to clinical trials.

Christiaan Leeuwenburgh, Thomas Buford, Maria Lorenzi … (2013)

Sarcopenia, the age-related loss of muscle mass and function, imposes a dramatic burden on individuals and society. The development of preventive and therapeutic strategies against sarcopenia is therefore perceived as an urgent need by health professionals and has instigated intensive research on the pathophysiology of this syndrome. The pathogenesis of sarcopenia is multifaceted and encompasses lifestyle habits, systemic factors (e.g., chronic inflammation and hormonal alterations), local environment perturbations (e.g., vascular dysfunction), and intramuscular specific processes. In this scenario, derangements in skeletal myocyte mitochondrial function are recognized as major factors contributing to the age-dependent muscle degeneration. In this review, we summarize prominent findings and controversial issues on the contribution of specific mitochondrial processes - including oxidative stress, quality control mechanisms and apoptotic signaling - on the development of sarcopenia. Extramuscular alterations accompanying the aging process with a potential impact on myocyte mitochondrial function are also discussed. We conclude with presenting methodological and safety considerations for the design of clinical trials targeting mitochondrial dysfunction to treat sarcopenia. Special emphasis is placed on the importance of monitoring the effects of an intervention on muscle mitochondrial function and identifying the optimal target population for the trial. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting. Copyright © 2013 Elsevier Ltd. All rights reserved.

0 comments Cited 218 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Redox regulation of SIRT1 in inflammation and cellular senescence.

Hongwei Yao, Isaac Sundar, Samuel Caito … (2013)

Sirtuin 1 (SIRT1) regulates inflammation, aging (life span and health span), calorie restriction/energetics, mitochondrial biogenesis, stress resistance, cellular senescence, endothelial functions, apoptosis/autophagy, and circadian rhythms through deacetylation of transcription factors and histones. SIRT1 level and activity are decreased in chronic inflammatory conditions and aging, in which oxidative stress occurs. SIRT1 is regulated by a NAD(+)-dependent DNA repair enzyme, poly(ADP-ribose) polymerase-1 (PARP1), and subsequent NAD(+) depletion by oxidative stress may have consequent effects on inflammatory and stress responses as well as cellular senescence. SIRT1 has been shown to undergo covalent oxidative modifications by cigarette smoke-derived oxidants/aldehydes, leading to posttranslational modifications, inactivation, and protein degradation. Furthermore, oxidant/carbonyl stress-mediated reduction of SIRT1 leads to the loss of its control on acetylation of target proteins including p53, RelA/p65, and FOXO3, thereby enhancing the inflammatory, prosenescent, and apoptotic responses, as well as endothelial dysfunction. In this review, the mechanisms of cigarette smoke/oxidant-mediated redox posttranslational modifications of SIRT1 and its roles in PARP1 and NF-κB activation, and FOXO3 and eNOS regulation, as well as chromatin remodeling/histone modifications during inflammaging, are discussed. Furthermore, we have also discussed various novel ways to activate SIRT1 either directly or indirectly, which may have therapeutic potential in attenuating inflammation and premature senescence involved in chronic lung diseases. Copyright © 2013 Elsevier Inc. All rights reserved.

0 comments Cited 204 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Journal

Journal ID (nlm-ta): Exp Ther Med

Journal ID (iso-abbrev): Exp Ther Med

Journal ID (publisher-id): ETM

Title: Experimental and Therapeutic Medicine

Publisher: D.A. Spandidos

ISSN (Print): 1792-0981

ISSN (Electronic): 1792-1015

Publication date (Print): July 2021

Publication date (Electronic): 02 May 2021

Publication date PMC-release: 02 May 2021

Volume: 22

Issue: 1

Electronic Location Identifier: 695

Affiliations

[1 ]College of Clinical Medicine, North China University of Science and Technology, Tangshan, Hebei 063000, P.R. China

[2 ]Department of Neurosurgery, The Affiliated Hospital of North China University of Science and Technology, Tangshan, Hebei 063000, P.R. China

[3 ]College of Nursing and Rehabilitation, North China University of Science and Technology, Tangshan, Hebei 063000, P.R. China

Author notes

Correspondence to: Dr Jianmin Li, College of Clinical Medicine, North China University of Science and Technology, 57 Jianshe South Road, Tangshan, Hebei 063000, P.R. China linchuangwangyc@ 123456ncst.edu.cn

Dr Yaning Zhao, College of Nursing and Rehabilitation, North China University of Science and Technology, 21 Bohai Avenue, Tangshan, Hebei 063000, P.R. China linchuangwangjy@ 123456ncst.edu.cn

Article

Publisher ID: ETM-0-0-10127

DOI: 10.3892/etm.2021.10127

PMC ID: 8111876

PubMed ID: 33986859

SO-VID: 89e0d387-b5dc-4008-9c89-5b7b40ae3999

License:

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

History

Date received : 09 November 2019

Date accepted : 02 September 2020

Funding

Funding: The present study was supported by the Hebei Medical Science Research Project, China (grant no. 20190106); the Tangshan City Science and Technology Project, China (grant no. 18130232a); and the North China University of Science and Technology Research and Research Project (grant no. Z201736).

Hypoxic postconditioning-induced neuroprotection increases neuronal autophagy via activation of the SIRT1/FoxO1 signaling pathway in rats with global cerebral ischemia

Read this article at

Abstract

Related collections

Neuronal Signaling

Most cited references 53

Autophagy: process and function.

Mitochondrial dysfunction and sarcopenia of aging: from signaling pathways to clinical trials.

Redox regulation of SIRT1 in inflammation and cellular senescence.

Author and article information

Journal

Affiliations

Author notes

Article

History

Funding

Categories

Comments

Comment on this article

Similar content 260

Cited by 4

Most referenced authors 741