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Cell non-autonomous proteostasis regulation in aging and disease

2022-06-09Artigo científico Acesso aberto
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dc.contributor.authorFerreira, Joao Vasco
dc.contributor.authorda Rosa Soares, Ana
dc.contributor.authorPereira, Paulo
dc.contributor.institutionCentro de Estudos de Doenças Crónicas (CEDOC)
dc.contributor.institutionNOVA Medical School|Faculdade de Ciências Médicas (NMS|FCM)
dc.contributor.pblFrontiers Media
dc.date.accessioned2022-09-22T22:37:30Z
dc.date.available2022-09-22T22:37:30Z
dc.date.issued2022-06-09
dc.descriptionFunding: This study was supported by the “Programa Operacional Regional de Lisboa-FEDER/ Project 02/SAICT/2020/072552,” and iNOVA4Health – UIDB/04462/2020 and UIDP/04462/2020, and by the Associated Laboratory LS4FUTURE (LA/P/0087/2020), two programs financially supported by Fundação para a Ciência e Tecnologia / Ministério da Ciência, Tecnologia e Ensino Superior.
dc.description.abstractAging is a risk factor for a number of diseases, being the more notorious ones perhaps neurodegenerative diseases such as Alzheimer's and Parkinson's. These and other age-related pathologies are often associated with accumulation of proteotoxic material inside cells, as well as with the accumulation of protein deposits extracellularly. It is widely accepted that this accumulation of toxic proteins trails a progressive decline in the mechanisms that regulate protein homeostasis, or proteostasis, during aging. However, despite significant efforts, the progress in terms of novel or improved therapies targeting accumulation of proteotoxic material has been rather limited. For example, clinical trials for new drugs aimed at treating Alzheimer's disease, by preventing accumulation of toxic proteins, have notoriously failed. On the other hand, it is becoming increasingly apparent that regulation of proteostasis is not a cell autonomous process. In fact, cells rely on complex transcellular networks to maintain tissue and organ homeostasis involving endocrine and paracrine signaling pathways. In this review we will discuss the impact of cell non-autonomous proteostasis mechanisms and their impact in aging and disease. We will focus on how transcellular proteostasis networks can shed new light into stablished paradigms about the aging of organisms.en
dc.description.versionpublishersversion
dc.description.versionpublished
dc.format.extent699949
dc.identifier.doi10.3389/fnins.2022.878296
dc.identifier.issn1662-4548
dc.identifier.otherPURE: 46538098
dc.identifier.otherPURE UUID: a055c4a0-6bd0-4a9e-ab8a-4968a9fb7557
dc.identifier.otherRIS: urn:308C19C62CB68AF0413C8ABE7751717D
dc.identifier.otherPubMed: 35757551
dc.identifier.otherWOS: 000815032700001
dc.identifier.otherScopus: 85140297594
dc.identifier.otherORCID: /0000-0002-9908-2290/work/151406799
dc.identifier.urihttp://hdl.handle.net/10362/143972
dc.identifier.urlhttps://www.ncbi.nlm.nih.gov/pubmed/35757551
dc.identifier.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9220288
dc.language.isoeng
dc.peerreviewedyes
dc.subjectmisfolding
dc.subjectmolecular chaperones
dc.subjectproteostasis
dc.subjectproteotoxicity
dc.subjecttranscellular
dc.titleCell non-autonomous proteostasis regulation in aging and diseaseen
dc.typejournal article
degois.publication.titleFrontiers in Cellular Neuroscience
degois.publication.volume16
dspace.entity.typePublication
rcaap.rightsopenAccess

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