ArticleTransplantation direct2016
The Role of Activin A and B and the Benefit of Follistatin Treatment in Renal Ischemia-Reperfusion Injury in Mice.
Article in Transplantation direct, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- The crystal structure of the activin B:Fst288 complex and computational insights into the broad antagonistic activity and specificity of follistatin.The Journal of biological chemistry · 2026Article
- The crystal structure of the activin B:Fst288 complex and computational insights into the broad antagonistic activity and specificity of follistatin.bioRxiv : the preprint server for biology · 2025Article
- Comprehensive molecular and cellular characterization of endoplasmic reticulum stress-related key genes in renal ischemia/reperfusion injury.Frontiers in immunology · 2024Article
- The Delivery of the Recombinant Protein Cocktail Identified by Stem Cell-Derived Secretome Analysis Accelerates Kidney Repair After Renal Ischemia-Reperfusion Injury.Frontiers in bioengineering and biotechnology · 2022Article
- miR299a-5p promotes renal fibrosis by suppressing the antifibrotic actions of follistatin.Scientific reports · 2021Article
- The Nephroprotective Effect of Lycopene on Renal Ischemic Reperfusion Injury: A Mouse Model.Indian journal of clinical biochemistry : IJCB · 2020Article
- Controlled Delivery of Stem Cell-Derived Trophic Factors Accelerates Kidney Repair After Renal Ischemia-Reperfusion Injury in Rats.Stem cells translational medicine · 2019Article
- Bioactive Compounds for the Treatment of Renal Disease.Yonsei medical journal · 2018Review
- Activin Biology After Lung Transplantation.Transplantation direct · 2017Article
- Activin B is a novel biomarker for chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) diagnosis: a cross sectional study.Journal of translational medicine · 2017Observational
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundActivins, members of the TGF-β superfamily, are key drivers of inflammation and are thought to play a significant role in ischemia-reperfusion injury (IRI), a process inherent to renal transplantation that negatively impacts early and late allograft function. Follistatin (FS) is a protein that binds activin and inhibits its activity. This study examined the response of activin A and B in mice after renal IRI and the effect of exogenous FS in modulating the severity of renal injury.
methodsMice were treated with recombinant FS288 or vehicle before renal IRI surgery. Activin A, B, and FS levels in the serum and kidney, and renal injury parameters were measured at 3, 6, and 24 hours after reperfusion.
resultsSerum and kidney activin B levels were increased within 6 hours postrenal IRI, accompanied by renal injury-increased serum creatinine, messenger (m)RNA expression of kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL); endothelial activation-increased E-selectin mRNA; and systemic inflammation-increased serum levels of IL-6, monocyte chemotactic protein-1 and TNF-α. Further injury was potentiated by an upsurge in activin A by 24 hours, with further increases in serum creatinine, KIM-1 and NGAL mRNA expression. Follistatin treatment significantly reduced the level of serum activin B and subsequently blunted the increase in activin A. Renoprotection was evident with the attenuated rise in serum creatinine, KIM-1 and NGAL expression, tubular injury score, renal cell apoptosis, and serum IL-6 and monocyte chemotactic protein-1 levels.
conclusionsWe propose that activin B initiates and activin A potentiates renal injury after IRI. Follistatin treatment, through binding and neutralizing the actions of activin B and subsequently activin A, reduced renal IRI by minimizing endothelial cell activation and dampening the systemic inflammatory response. These data support the potential clinical application of FS treatment to limit IRI during renal transplantation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.