Gq signaling in autophagy control: between chemical and mechanical cues

All processes in human physiology relies on homeostatic mechanisms which require the activation of specific control circuits to adapt the changes imposed by external stimuli. One of the critical modulators of homeostatic balance is autophagy, a catabolic process that is responsible of the destructio...

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Authors: Navarro-Lérida, Inmaculada, Aragay, Anna M., Asensio, Alejandro, Ribas, Catalina
Format: article
Status:Published version
Publication Date:2022
Country:España
Institution:Consejo Superior de Investigaciones Científicas (CSIC)
Repository:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:digital.csic.es:10261/285417
Online Access:http://hdl.handle.net/10261/285417
Access Level:Open access
Keyword:GPCR
Gq
autophagy
Oxidative stress
Mechanotransduction
Extracellular matrix
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spelling Gq signaling in autophagy control: between chemical and mechanical cuesNavarro-Lérida, InmaculadaAragay, Anna M.Asensio, AlejandroRibas, CatalinaGPCRGqautophagyOxidative stressMechanotransductionExtracellular matrixAll processes in human physiology relies on homeostatic mechanisms which require the activation of specific control circuits to adapt the changes imposed by external stimuli. One of the critical modulators of homeostatic balance is autophagy, a catabolic process that is responsible of the destruction of long-lived proteins and organelles through a lysosome degradative pathway. Identification of the mechanism underlying autophagic flux is considered of great importance as both protective and detrimental functions are linked with deregulated autophagy. At the mechanistic and regulatory levels, autophagy is activated in response to diverse stress conditions (food deprivation, hyperthermia and hypoxia), even a novel perspective highlight the potential role of physical forces in autophagy modulation. To understand the crosstalk between all these controlling mechanisms could give us new clues about the specific contribution of autophagy in a wide range of diseases including vascular disorders, inflammation and cancer. Of note, any homeostatic control critically depends in at least two additional and poorly studied interdependent components: a receptor and its downstream effectors. Addressing the selective receptors involved in autophagy regulation is an open question and represents a new area of research in this field. G-protein coupled receptors (GPCRs) represent one of the largest and druggable targets membrane receptor protein superfamily. By exerting their action through G proteins, GPCRs play fundamental roles in the control of cellular homeostasis. Novel studies have shown Gαq, a subunit of heterotrimeric G proteins, as a core modulator of mTORC1 and autophagy, suggesting a fundamental contribution of Gαq-coupled GPCRs mechanisms in the control of this homeostatic feedback loop. To address how GPCR-G proteins machinery integrates the response to different stresses including oxidative conditions and mechanical stimuli, could provide deeper insight into new signaling pathways and open potential and novel therapeutic strategies in the modulation of different pathological conditions.Our work was supported by: Instituto de Salud Carlos III (PI18/01662 to CR, co-funded with European FEDER contribution), CIBERCV-Instituto de Salud Carlos III, Spain (grant CB16/11/00278, co-funded with European FEDER contribution), Fundación Ramón Areces (to CR). Ministerio de Economía; Industria y Competitividad (MINECO) of Spain (grant BFU2017-83379-R to AMA), COVTRAVI-19-CM (Comunidad de Madrid, co-funded with European FEDER contribution). We also acknowledge institutional support to the CBMSO from Fundación Ramón Areces.Multidisciplinary Digital Publishing InstituteInstituto de Salud Carlos IIIFundación Ramón ArecesMinisterio de Economía y Competitividad (España)Ministerio de Ciencia, Innovación y Universidades (España)Agencia Estatal de Investigación (España)Comunidad de MadridConsejo Superior de Investigaciones Científicas [https://ror.org/02gfc7t72]2022202220222022info:eu-repo/semantics/articlehttp://purl.org/coar/resource_type/c_dcae04bcPublisher's versioninfo:eu-repo/semantics/publishedVersionapplication/pdfhttp://hdl.handle.net/10261/285417reponame:DIGITAL.CSIC. Repositorio Institucional del CSICinstname:Consejo Superior de Investigaciones Científicas (CSIC)Inglés#PLACEHOLDER_PARENT_METADATA_VALUE#info:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2013-2016/BFU2017-83379-Rhttp://dx.doi.org/10.3390/antiox11081599Síinfo:eu-repo/semantics/openAccessoai:digital.csic.es:10261/2854172026-05-22T06:33:51Z
dc.title.none.fl_str_mv Gq signaling in autophagy control: between chemical and mechanical cues
title Gq signaling in autophagy control: between chemical and mechanical cues
spellingShingle Gq signaling in autophagy control: between chemical and mechanical cues
Navarro-Lérida, Inmaculada
GPCR
Gq
autophagy
Oxidative stress
Mechanotransduction
Extracellular matrix
title_short Gq signaling in autophagy control: between chemical and mechanical cues
title_full Gq signaling in autophagy control: between chemical and mechanical cues
title_fullStr Gq signaling in autophagy control: between chemical and mechanical cues
title_full_unstemmed Gq signaling in autophagy control: between chemical and mechanical cues
title_sort Gq signaling in autophagy control: between chemical and mechanical cues
dc.creator.none.fl_str_mv Navarro-Lérida, Inmaculada
Aragay, Anna M.
Asensio, Alejandro
Ribas, Catalina
author Navarro-Lérida, Inmaculada
author_facet Navarro-Lérida, Inmaculada
Aragay, Anna M.
Asensio, Alejandro
Ribas, Catalina
author_role author
author2 Aragay, Anna M.
Asensio, Alejandro
Ribas, Catalina
author2_role author
author
author
dc.contributor.none.fl_str_mv Instituto de Salud Carlos III
Fundación Ramón Areces
Ministerio de Economía y Competitividad (España)
Ministerio de Ciencia, Innovación y Universidades (España)
Agencia Estatal de Investigación (España)
Comunidad de Madrid
Consejo Superior de Investigaciones Científicas [https://ror.org/02gfc7t72]
dc.subject.none.fl_str_mv GPCR
Gq
autophagy
Oxidative stress
Mechanotransduction
Extracellular matrix
topic GPCR
Gq
autophagy
Oxidative stress
Mechanotransduction
Extracellular matrix
description All processes in human physiology relies on homeostatic mechanisms which require the activation of specific control circuits to adapt the changes imposed by external stimuli. One of the critical modulators of homeostatic balance is autophagy, a catabolic process that is responsible of the destruction of long-lived proteins and organelles through a lysosome degradative pathway. Identification of the mechanism underlying autophagic flux is considered of great importance as both protective and detrimental functions are linked with deregulated autophagy. At the mechanistic and regulatory levels, autophagy is activated in response to diverse stress conditions (food deprivation, hyperthermia and hypoxia), even a novel perspective highlight the potential role of physical forces in autophagy modulation. To understand the crosstalk between all these controlling mechanisms could give us new clues about the specific contribution of autophagy in a wide range of diseases including vascular disorders, inflammation and cancer. Of note, any homeostatic control critically depends in at least two additional and poorly studied interdependent components: a receptor and its downstream effectors. Addressing the selective receptors involved in autophagy regulation is an open question and represents a new area of research in this field. G-protein coupled receptors (GPCRs) represent one of the largest and druggable targets membrane receptor protein superfamily. By exerting their action through G proteins, GPCRs play fundamental roles in the control of cellular homeostasis. Novel studies have shown Gαq, a subunit of heterotrimeric G proteins, as a core modulator of mTORC1 and autophagy, suggesting a fundamental contribution of Gαq-coupled GPCRs mechanisms in the control of this homeostatic feedback loop. To address how GPCR-G proteins machinery integrates the response to different stresses including oxidative conditions and mechanical stimuli, could provide deeper insight into new signaling pathways and open potential and novel therapeutic strategies in the modulation of different pathological conditions.
publishDate 2022
dc.date.none.fl_str_mv 2022
2022
2022
2022
dc.type.none.fl_str_mv info:eu-repo/semantics/article
http://purl.org/coar/resource_type/c_dcae04bc
Publisher's version
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/10261/285417
url http://hdl.handle.net/10261/285417
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv #PLACEHOLDER_PARENT_METADATA_VALUE#
info:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2013-2016/BFU2017-83379-R
http://dx.doi.org/10.3390/antiox11081599
Sí
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Multidisciplinary Digital Publishing Institute
publisher.none.fl_str_mv Multidisciplinary Digital Publishing Institute
dc.source.none.fl_str_mv reponame:DIGITAL.CSIC. Repositorio Institucional del CSIC
instname:Consejo Superior de Investigaciones Científicas (CSIC)
instname_str Consejo Superior de Investigaciones Científicas (CSIC)
reponame_str DIGITAL.CSIC. Repositorio Institucional del CSIC
collection DIGITAL.CSIC. Repositorio Institucional del CSIC
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15.812429

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