TRAP1 in Oxidative Stress and Neurodegeneration

Tumor necrosis factor receptor-associated protein 1 (TRAP1), also known as heat shock protein 75 (HSP75), is a member of the heat shock protein 90 (HSP90) chaperone family that resides mainly in the mitochondria. As a mitochondrial molecular chaperone, TRAP1 supports protein folding and contributes...

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Autores principales:	Inês Ramos Rego, Beatriz Santos Cruz, António Francisco Ambrósio, Celso Henrique Alves
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	HSP75 HSP90 mitochondria neurodegeneration oxidative stress TRAP1 Therapeutics. Pharmacology RM1-950
Acceso en línea:	https://doaj.org/article/e349aa5b582f4ee5a50c916040ecc6ad
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spelling	oai:doaj.org-article:e349aa5b582f4ee5a50c916040ecc6ad2021-11-25T16:29:31ZTRAP1 in Oxidative Stress and Neurodegeneration10.3390/antiox101118292076-3921https://doaj.org/article/e349aa5b582f4ee5a50c916040ecc6ad2021-11-01T00:00:00Zhttps://www.mdpi.com/2076-3921/10/11/1829https://doaj.org/toc/2076-3921Tumor necrosis factor receptor-associated protein 1 (TRAP1), also known as heat shock protein 75 (HSP75), is a member of the heat shock protein 90 (HSP90) chaperone family that resides mainly in the mitochondria. As a mitochondrial molecular chaperone, TRAP1 supports protein folding and contributes to the maintenance of mitochondrial integrity even under cellular stress. TRAP1 is a cellular regulator of mitochondrial bioenergetics, redox homeostasis, oxidative stress-induced cell death, apoptosis, and unfolded protein response (UPR) in the endoplasmic reticulum (ER). TRAP1 has attracted increasing interest as a therapeutical target, with a special focus on the design of TRAP1 specific inhibitors. Although TRAP1 was extensively studied in the oncology field, its role in central nervous system cells, under physiological and pathological conditions, remains largely unknown. In this review, we will start by summarizing the biology of TRAP1, including its structure and related pathways. Thereafter, we will continue by debating the role of TRAP1 in the maintenance of redox homeostasis and protection against oxidative stress and apoptosis. The role of TRAP1 in neurodegenerative disorders will also be discussed. Finally, we will review the potential of TRAP1 inhibitors as neuroprotective drugs.Inês Ramos RegoBeatriz Santos CruzAntónio Francisco AmbrósioCelso Henrique AlvesMDPI AGarticleHSP75HSP90mitochondrianeurodegenerationoxidative stressTRAP1Therapeutics. PharmacologyRM1-950ENAntioxidants, Vol 10, Iss 1829, p 1829 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	HSP75 HSP90 mitochondria neurodegeneration oxidative stress TRAP1 Therapeutics. Pharmacology RM1-950
spellingShingle	HSP75 HSP90 mitochondria neurodegeneration oxidative stress TRAP1 Therapeutics. Pharmacology RM1-950 Inês Ramos Rego Beatriz Santos Cruz António Francisco Ambrósio Celso Henrique Alves TRAP1 in Oxidative Stress and Neurodegeneration
description	Tumor necrosis factor receptor-associated protein 1 (TRAP1), also known as heat shock protein 75 (HSP75), is a member of the heat shock protein 90 (HSP90) chaperone family that resides mainly in the mitochondria. As a mitochondrial molecular chaperone, TRAP1 supports protein folding and contributes to the maintenance of mitochondrial integrity even under cellular stress. TRAP1 is a cellular regulator of mitochondrial bioenergetics, redox homeostasis, oxidative stress-induced cell death, apoptosis, and unfolded protein response (UPR) in the endoplasmic reticulum (ER). TRAP1 has attracted increasing interest as a therapeutical target, with a special focus on the design of TRAP1 specific inhibitors. Although TRAP1 was extensively studied in the oncology field, its role in central nervous system cells, under physiological and pathological conditions, remains largely unknown. In this review, we will start by summarizing the biology of TRAP1, including its structure and related pathways. Thereafter, we will continue by debating the role of TRAP1 in the maintenance of redox homeostasis and protection against oxidative stress and apoptosis. The role of TRAP1 in neurodegenerative disorders will also be discussed. Finally, we will review the potential of TRAP1 inhibitors as neuroprotective drugs.
format	article
author	Inês Ramos Rego Beatriz Santos Cruz António Francisco Ambrósio Celso Henrique Alves
author_facet	Inês Ramos Rego Beatriz Santos Cruz António Francisco Ambrósio Celso Henrique Alves
author_sort	Inês Ramos Rego
title	TRAP1 in Oxidative Stress and Neurodegeneration
title_short	TRAP1 in Oxidative Stress and Neurodegeneration
title_full	TRAP1 in Oxidative Stress and Neurodegeneration
title_fullStr	TRAP1 in Oxidative Stress and Neurodegeneration
title_full_unstemmed	TRAP1 in Oxidative Stress and Neurodegeneration
title_sort	trap1 in oxidative stress and neurodegeneration
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/e349aa5b582f4ee5a50c916040ecc6ad
work_keys_str_mv	AT inesramosrego trap1inoxidativestressandneurodegeneration AT beatrizsantoscruz trap1inoxidativestressandneurodegeneration AT antoniofranciscoambrosio trap1inoxidativestressandneurodegeneration AT celsohenriquealves trap1inoxidativestressandneurodegeneration
_version_	1718413171439435776

TRAP1 in Oxidative Stress and Neurodegeneration

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