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Leptin signaling in obesity and colorectal cancer

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dc.contributor.authorTerezia Socol, Claudia
dc.contributor.authorChira, Alexandra
dc.contributor.authorMartínez-Sánchez, Maria Antonia
dc.contributor.authorNuñez-Sánchez, MarÍa Ángeles
dc.contributor.authorMaerescu, Cristina María
dc.contributor.authorMierlita, Daniel
dc.contributor.authorVasile Rusu, Alexandru
dc.contributor.authorRuiz Alcaraz, Antonio José
dc.contributor.authorTrif, Mónica
dc.contributor.authorRamos-Molina, Bruno
dc.contributor.departmentBioquímica y Biología Molecular B e Inmunología
dc.contributor.otherFacultad de Biología
dc.date.accessioned2026-01-14T11:20:05Z
dc.date.available2026-01-14T11:20:05Z
dc.date.copyright© 2022 by the authors
dc.date.issued2022-04-24
dc.description.abstractObesity and colorectal cancer (CRC) are among the leading diseases causing deaths in the world, showing a complex multifactorial pathology. Obesity is considered a risk factor in CRC development through inflammation, metabolic, and signaling processes. Leptin is one of the most important adipokines related to obesity and an important proinflammatory marker, mainly expressed in adipose tissue, with many genetic variation profiles, many related influencing factors, and various functions that have been ascribed but not yet fully understood and elucidated, the most important ones being related to energy metabolism, as well as endocrine and immune systems. Aberrant signaling and genetic variations of leptin are correlated with obesity and CRC, with the genetic causality showing both inherited and acquired events, in addition to lifestyle and environmental risk factors; these might also be related to specific pathogenic pathways at different time points. Moreover, mutation gain is a crucial factor enabling the genetic process of CRC. Currently, the inconsistent and insufficient data related to leptin’s relationship with obesity and CRC indicate the necessity of further related studies. This review summarizes the current knowledge on leptin genetics and its potential relationship with the main pathogenic pathways of obesity and CRC, in an attempt to understand the molecular mechanisms of these associations, in the context of inconsistent and contradictory data. The understanding of these mechanisms linking obesity and CRC could help to develop novel therapeutic targets and prevention strategies, resulting in a better prognosis and management of these diseases.
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dc.format.extent21
dc.identifier.citationInt. J. Mol. Sci. 2022, 23, 4713
dc.identifier.doihttps://doi.org/10.3390/ijms23094713
dc.identifier.eissn1422-0067
dc.identifier.issn1661-6596
dc.identifier.urihttp://hdl.handle.net/10201/186809
dc.languageeng
dc.publisherMDPI
dc.relationThis work was funded by the Institute of Health “Carlos III” (ISCIII) and co-funded by the Fondo Europeo de Desarrollo Regional-FEDER (grant number PI20/00505). B.R.-M. was supported by the “Miguel Servet Type I” program (CP19/00098, ISCIII, Spain; co-funded by the Fondo Europeo de Desarrollo Regional-FEDER). M.A.M.-S. was supported by a PFIS contract from the IISCIII (FI21/00003, ISCIII, Spain; co-funded by the Fondo Europeo de Desarrollo Regional-FEDER).
dc.relation.publisherversionhttps://www.mdpi.com/1422-0067/23/9/4713
dc.rightsAttribution 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectLEPR
dc.subjectObesity
dc.subjectColorectal cancer
dc.subjectMicrobiome
dc.subjectLEP
dc.subject.odsNo relacionado con ningún objetivo de desarrollo sostenible
dc.titleLeptin signaling in obesity and colorectal cancer
dc.typeinfo:eu-repo/semantics/article
dc.type.versioninfo:eu-repo/semantics/publishedVersion
dspace.entity.typePublicationes
relation.isAuthorOfPublicationc5d54ef3-bd3b-4330-b4a1-252ab278925b
relation.isAuthorOfPublication.latestForDiscoveryc5d54ef3-bd3b-4330-b4a1-252ab278925b
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