Target Sestrin2 to Rescue the Damaged Organ: Mechanistic Insight into Its Function

Sestrin2 is a stress-inducible metabolic regulator and a conserved antioxidant protein which has been implicated in the pathogenesis of several diseases. Sestrin2 can protect against atherosclerosis, heart failure, hypertension, myocardial infarction, stroke, spinal cord injury neurodegeneration, no...

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Autores principales:	Moein Ala, Seyed Parsa Eftekhar
Formato:	article
Lenguaje:	EN
Publicado:	Hindawi Limited 2021
Materias:	Cytology QH573-671
Acceso en línea:	https://doaj.org/article/b7df3e5b97764f93a9b434b5d10f464c
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spelling	oai:doaj.org-article:b7df3e5b97764f93a9b434b5d10f464c2021-11-15T01:19:08ZTarget Sestrin2 to Rescue the Damaged Organ: Mechanistic Insight into Its Function1942-099410.1155/2021/8790369https://doaj.org/article/b7df3e5b97764f93a9b434b5d10f464c2021-01-01T00:00:00Zhttp://dx.doi.org/10.1155/2021/8790369https://doaj.org/toc/1942-0994Sestrin2 is a stress-inducible metabolic regulator and a conserved antioxidant protein which has been implicated in the pathogenesis of several diseases. Sestrin2 can protect against atherosclerosis, heart failure, hypertension, myocardial infarction, stroke, spinal cord injury neurodegeneration, nonalcoholic fatty liver disease (NAFLD), liver fibrosis, acute kidney injury (AKI), chronic kidney disease (CKD), and pulmonary inflammation. Oxidative stress and cellular damage signals can alter the expression of Sestrin2 to compensate for organ damage. Different stress signals such as those mediated by P53, Nrf2/ARE, HIF-1α, NF-κB, JNK/c-Jun, and TGF-β/Smad signaling pathways can induce Sestrin2 expression. Subsequently, Sestrin2 activates Nrf2 and AMPK. Furthermore, Sestrin2 is a major negative regulator of mTORC1. Sestrin2 indirectly regulates the expression of several genes and reprograms intracellular signaling pathways to attenuate oxidative stress and modulate a large number of cellular events such as protein synthesis, cell energy homeostasis, mitochondrial biogenesis, autophagy, mitophagy, endoplasmic reticulum (ER) stress, apoptosis, fibrogenesis, and lipogenesis. Sestrin2 vigorously enhances M2 macrophage polarization, attenuates inflammation, and prevents cell death. These alterations in molecular and cellular levels improve the clinical presentation of several diseases. This review will shed light on the beneficial effects of Sestrin2 on several diseases with an emphasis on underlying pathophysiological effects.Moein AlaSeyed Parsa EftekharHindawi LimitedarticleCytologyQH573-671ENOxidative Medicine and Cellular Longevity, Vol 2021 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Cytology QH573-671
spellingShingle	Cytology QH573-671 Moein Ala Seyed Parsa Eftekhar Target Sestrin2 to Rescue the Damaged Organ: Mechanistic Insight into Its Function
description	Sestrin2 is a stress-inducible metabolic regulator and a conserved antioxidant protein which has been implicated in the pathogenesis of several diseases. Sestrin2 can protect against atherosclerosis, heart failure, hypertension, myocardial infarction, stroke, spinal cord injury neurodegeneration, nonalcoholic fatty liver disease (NAFLD), liver fibrosis, acute kidney injury (AKI), chronic kidney disease (CKD), and pulmonary inflammation. Oxidative stress and cellular damage signals can alter the expression of Sestrin2 to compensate for organ damage. Different stress signals such as those mediated by P53, Nrf2/ARE, HIF-1α, NF-κB, JNK/c-Jun, and TGF-β/Smad signaling pathways can induce Sestrin2 expression. Subsequently, Sestrin2 activates Nrf2 and AMPK. Furthermore, Sestrin2 is a major negative regulator of mTORC1. Sestrin2 indirectly regulates the expression of several genes and reprograms intracellular signaling pathways to attenuate oxidative stress and modulate a large number of cellular events such as protein synthesis, cell energy homeostasis, mitochondrial biogenesis, autophagy, mitophagy, endoplasmic reticulum (ER) stress, apoptosis, fibrogenesis, and lipogenesis. Sestrin2 vigorously enhances M2 macrophage polarization, attenuates inflammation, and prevents cell death. These alterations in molecular and cellular levels improve the clinical presentation of several diseases. This review will shed light on the beneficial effects of Sestrin2 on several diseases with an emphasis on underlying pathophysiological effects.
format	article
author	Moein Ala Seyed Parsa Eftekhar
author_facet	Moein Ala Seyed Parsa Eftekhar
author_sort	Moein Ala
title	Target Sestrin2 to Rescue the Damaged Organ: Mechanistic Insight into Its Function
title_short	Target Sestrin2 to Rescue the Damaged Organ: Mechanistic Insight into Its Function
title_full	Target Sestrin2 to Rescue the Damaged Organ: Mechanistic Insight into Its Function
title_fullStr	Target Sestrin2 to Rescue the Damaged Organ: Mechanistic Insight into Its Function
title_full_unstemmed	Target Sestrin2 to Rescue the Damaged Organ: Mechanistic Insight into Its Function
title_sort	target sestrin2 to rescue the damaged organ: mechanistic insight into its function
publisher	Hindawi Limited
publishDate	2021
url	https://doaj.org/article/b7df3e5b97764f93a9b434b5d10f464c
work_keys_str_mv	AT moeinala targetsestrin2torescuethedamagedorganmechanisticinsightintoitsfunction AT seyedparsaeftekhar targetsestrin2torescuethedamagedorganmechanisticinsightintoitsfunction
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Target Sestrin2 to Rescue the Damaged Organ: Mechanistic Insight into Its Function

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