ArticleSurgery2018
GDF11 induces kidney fibrosis, renal cell epithelial-to-mesenchymal transition, and kidney dysfunction and failure.
Article in Surgery, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Ift46 deficiency causes renal cyst via enhanced Limk2 through lack of autophagy flux.Cell communication and signaling : CCS · 2026Article
- GDF11-secreting cell transplant efficiently ameliorates age-related pulmonary fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- gdf11 is required for pronephros/cloaca development through targeting TGF-β signaling.Scientific reports · 2025Article
- GDF-15 Attenuates the Epithelium-Mesenchymal Transition and Alleviates TGFβ2-Induced Lens Opacity.Translational vision science & technology · 2024Article
- GDF11, a target of miR-32-5p, suppresses high-glucose-induced mitochondrial dysfunction and apoptosis in HK-2 cells through PI3K/AKT signaling activation.International urology and nephrology · 2023Article
- Deficiency of GDF-11 Accelerates TAC-Induced Heart Failure by Impairing Cardiac Angiogenesis.JACC. Basic to translational science · 2023Article
- Loss of MEN1 leads to renal fibrosis and decreases HGF-Adamts5 pathway activity via an epigenetic mechanism.Clinical and translational medicine · 2022Article
- Myostatin/Activin Receptor Ligands in Muscle and the Development Status of Attenuating Drugs.Endocrine reviews · 2022Review
- Exosomes derived from mesenchymal stem cells ameliorate renal fibrosis via delivery of miR-186-5p.Human cell · 2022Article
- Follistatin Attenuates Myocardial Fibrosis in Diabetic CardiomyopathyFrontiers in pharmacology · 2021Article
- Candidate rejuvenating factor GDF11 and tissue fibrosis: friend or foe?GeroScience · 2020Review
- Similar sequences but dissimilar biological functions of GDF11 and myostatin.Experimental & molecular medicine · 2020Review
- Growth differentiation factor 11 promotes differentiation of MSCs into endothelial-like cells for angiogenesis.Journal of cellular and molecular medicine · 2020Article
- Growth differentiation factor 11 inhibits adipogenic differentiation by activating TGF-beta/Smad signalling pathway.Cell proliferation · 2019Article
- Oxalate induces type II epithelial to mesenchymal transition (EMT) in inner medullary collecting duct cells (IMCD)Oncotarget · 2019Article
- miRNAs in Extracellular Vesicles from iPS-Derived Cardiac Progenitor Cells Effectively Reduce Fibrosis and Promote Angiogenesis in Infarcted Heart.Stem cells international · 2019Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundGDF11 modulates embryonic patterning and kidney organogenesis. Herein, we sought to define GDF11 function in the adult kidney and in renal diseases.
methodsIn vitro renal cell lines, genetic, and murine in vivo renal injury models were examined.
resultsAmong tissues tested, Gdf11 was highest in normal adult mouse kidney. Expression was increased acutely after 5/6 nephrectomy, ischemia-reperfusion injury, kanamycin toxicity, or unilateral ureteric obstruction. Systemic, high-dose GDF11 administration in adult mice led to renal failure, with accompanying kidney atrophy, interstitial fibrosis, epithelial-to-mesenchymal transition of renal tubular cells, and eventually death. These effects were associated with phosphorylation of SMAD2 and could be blocked by follistatin. In contrast, Gdf11 heterozygous mice showed reduced renal Gdf11 expression, renal fibrosis, and expression of fibrosis-associated genes both at baseline and after unilateral ureteric obstruction compared with wild-type littermates. The kidney-specific consequences of GDF11 dose modulation are direct effects on kidney cells. GDF11 induced proliferation and activation of NRK49f renal fibroblasts and also promoted epithelial-to-mesenchymal transition of IMCD-3 tubular epithelial cells in a SMAD3-dependent manner.
conclusionTaken together, these data suggest that GDF11 and its downstream signals are critical in vivo mediators of renal injury. These effects are through direct actions of GDF11 on renal tubular cells and fibroblasts. Thus, regulation of GDF11 presents a therapeutic target for diseases involving renal fibrosis and impaired tubular function.
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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.