ArticleIn vitro cellular & developmental biology. Animal2018
HIF1α deletion facilitates adipose stem cells to repair renal fibrosis in diabetic mice.
Article in In vitro cellular & developmental biology. Animal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.
- A systematic review and meta-analysis of cell-based interventions in experimental diabetic kidney disease.Stem cells translational medicine · 2021Pooled it
- Stem cell-based treatment of kidney diseases.Experimental biology and medicine (Maywood, N.J.) · 2020Review
- HIF1α overexpression enhances diabetic wound closure in high glucose and low oxygen conditions by promoting adipose-derived stem cell paracrine function and survival.Stem cell research & therapy · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Adipose stem cell (ASC) transplantation is a promising therapeutic strategy for diabetic renal fibrosis. Hypoxia-inducible factor 1α (HIF1α) is a negative regulatory factor of mitochondrial function. In the current study, we aimed to explore if HIF1α deletion protects against hyperglycemia-induced ASC damage and enhances the therapeutic efficiency of ASCs in diabetic renal fibrosis. Our data indicated that HIF1α was upregulated in ASCs in response to high glucose stimulation. Higher HIF1α expression was associated with ASC apoptosis and proliferation arrest. Loss of HIF1α activated mitophagy protecting ASCs against high glucose-induced apoptosis via preserving mitochondrial function. Transplanting HIF1α-deleted ASCs in db/db mice improved the abnormalities in glucose metabolic parameters, including the levels of glucose, insulin, C-peptide, HbA1c, and inflammatory markers. In addition, the engraftment of HIF1α-modified ASCs also reversed renal function, decreased renal hypertrophy, and ameliorated renal histological changes in db/db mice. Functional studies confirmed that HIF1α-modified ASCs reduced renal fibrosis. Collectively, our results demonstrate that ASCs may be a promising therapeutic treatment for ameliorating diabetes and the development of renal fibrosis and that the loss of HIF1α in ASCs may further increase the efficiency of stem cell-based therapy. These findings provide a new understanding about the protective effects of HIF1α silencing on ASCs and offer a new strategy for promoting the therapeutic efficacy of ASCs in diabetic renal fibrosis.
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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.