Galectin-8 counteracts folic acid-induced acute kidney injury and prevents its transition to fibrosis

Simple item page
dc.contributor.authorPerez-Moreno, Elisa
dc.contributor.authorToledo, Tomas
dc.contributor.authorCampusano, Pascale
dc.contributor.authorZuniga, Sebastian
dc.contributor.authorAzocar, Lorena
dc.contributor.authorFeuerhake, Teo
dc.contributor.authorMendez, Gonzalo P.
dc.contributor.authorLabarca, Mariana
dc.contributor.authorPerez-Molina, Francisca
dc.contributor.authorde la Pena, Adely
dc.contributor.authorHerrera-Cid, Cristian
dc.contributor.authorEhrenfeld, Pamela
dc.contributor.authorGodoy, Alejandro S.
dc.contributor.authorGonzalez, Alfonso
dc.contributor.authorSoza, Andrea
dc.date.accessioned2025-01-20T16:14:11Z
dc.date.available2025-01-20T16:14:11Z
dc.date.issued2024
dc.description.abstractAcute kidney injury (AKI), characterized by a sudden decline in kidney function involving tubular damage and epithelial cell death, can lead to progressive tissue fibrosis and chronic kidney disease due to interstitial fibroblast activation and tissue repair failures that lack direct treatments. After an AKI episode, surviving renal tubular cells undergo cycles of dedifferentiation, proliferation and redifferentiation while fibroblast activity increases and then declines to avoid an exaggerated extracellular matrix deposition. Appropriate tissue recovery versus pathogenic fibrotic progression depends on fine-tuning all these processes. Identifying endogenous factors able to affect any of them may offer new therapeutic opportunities to improve AKI outcomes. Galectin-8 (Gal-8) is an endogenous carbohydrate-binding protein that is secreted through an unconventional mechanism, binds to glycosylated proteins at the cell surface and modifies various cellular activities, including cell proliferation and survival against stress conditions. Here, using a mouse model of AKI induced by folic acid, we show that pretreatment with Gal-8 protects against cell death, promotes epithelial cell redifferentiation and improves renal function. In addition, Gal-8 decreases fibroblast activation, resulting in less expression of fibrotic genes. Gal-8 added after AKI induction is also effective in maintaining renal function against damage, improving epithelial cell survival. The ability to protect kidneys from injury during both pre- and post-treatments, coupled with its anti-fibrotic effect, highlights Gal-8 as an endogenous factor to be considered in therapeutic strategies aimed at improving renal function and mitigating chronic pathogenic progression.
dc.fuente.origenWOS
dc.identifier.doi10.1016/j.biopha.2024.116923
dc.identifier.eissn1950-6007
dc.identifier.issn0753-3322
dc.identifier.urihttps://doi.org/10.1016/j.biopha.2024.116923
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/90427
dc.identifier.wosidWOS:001261118000001
dc.language.isoen
dc.revistaBiomedicine & pharmacotherapy
dc.rightsacceso restringido
dc.subjectAcute kidney injury
dc.subjectGalectin-8
dc.subjectFolic acid
dc.subjectEpithelial-mesenchymal transition
dc.subjectEpithelial-mesenchymal plasticity
dc.subjectAKI-to-CKD transition
dc.subjectFibrosis
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleGalectin-8 counteracts folic acid-induced acute kidney injury and prevents its transition to fibrosis
dc.typeartículo
dc.volumen177
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
Files
Collections
Artículos de revistas