ArticleMolecular medicine (Cambridge, Mass.)2018
Reversal of angiotensin ll-induced β-cell dedifferentiation via inhibition of NF-κb signaling.
Article in Molecular medicine (Cambridge, Mass.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 31 citations in OpenAlex.
- The Effect of Angiotensin (1-7) on Serum Metabolomics in Obese Type 2 Diabetic Mice.Metabolites · 2026Article
- TBL1X/TBL1XR1 govern β-cell identity through a PAX6-containing gene regulatory network.Nature communications · 2026Article
- Combined Metformin and Baricitinib Therapy Attenuates Inflammation in STZ-Induced Diabetic Rats via AMPK/JAK-STAT Pathway Crosstalk.Endocrinology, diabetes & metabolism · 2025Article
- Ras homolog enriched in brain 1 regulates β cell mass and β cell functionWorld journal of diabetes · 2025Article
- Rescuing vascular dysfunction in dorsal pancreatic arteries prevents tacrolimus-induced glucose metabolism disorder in mice.Molecular medicine (Cambridge, Mass.) · 2025Article
- Small RNA-Seq and real time rt-qPCR reveal islet miRNA released under stress conditions.Islets · 2024Article
- Protective Effects of Berberine on Nonalcoholic Fatty Liver Disease in db/db Mice via AMPK/SIRT1 Pathway Activation.Current medical science · 2024Article
- Targeting β-Cell Plasticity: A Promising Approach for Diabetes Treatment.Current issues in molecular biology · 2024Review
- Novel lipid mediator 7Frontiers in cell and developmental biology · 2024Article
- Long-Term Administration of Omeprazole-Induced Hypergastrinemia and Changed Glucose Homeostasis and Expression of Metabolism-Related Genes.BioMed research international · 2024Article
- The Counteracting Effects of Ang II and Ang-(1-7) on the Function andGrowth of Insulin-secreting NIT-1 Cells.Current diabetes reviews · 2024Article
- Prolonged activation of NMDA receptors induces dedifferentiation of islet β cells in mice.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022Article
- Adipose Tissue Secretion Pattern Influences β-Cell Wellness in the Transition from Obesity to Type 2 Diabetes.International journal of molecular sciences · 2022Review
- The Plasticity of Pancreatic β-Cells.Metabolites · 2021Review
- Pancreatic β cell regeneration induced by clinical and preclinical agents.World journal of stem cells · 2021Review
- Probiotic mediated NF-κB regulation for prospective management of type 2 diabetes.Molecular biology reports · 2020Review
- Is Atorvastatin Associated with New Onset Diabetes or Deterioration of Glycemic Control? Systematic Review Using Data from 1.9 Million Patients.International journal of endocrinology · 2018Review
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9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundType 2 diabetes mellitus (T2DM) is characterized by pancreatic β-cell failure, which arises from metabolic stress and results in β cell dedifferentiation, leading to β-cell death. Pathological activation of the renin-angiotensin system (RAS) contributes to increase cell stress, while RAS intervention reduces the onset of T2DM in high-risk populations and promotes insulin secretion in rodents. In this study, we investigated whether and how RAS induces β-cell dedifferentiation and the mechanism underlying this process.
methodsIn vitro, with the methods of quantitative real-time reverse transcriptase-PCR (qRT-PCR) and western blotting, we examined the change of cell identity-related gene expression, progenitor like gene expression, cellular function, and nuclear factor kappa b (NF-κb) signaling activity in β cell lines after exposure to angiotensin II (AngII) and disruption of RAS. In vivo, parallel studies were performed using db/db mice. Related protein expression was detected by Immunofluorescence analysis.
resultActivation of RAS induced dedifferentiation and impaired insulin secretion, eventually leading to β-cell failure. Mechanistically, Angll induced β-cell dedifferentiation via NF-κb signaling, while treatment with lrbesartan and sc-514 reversed the progenitor state of β cells.
conclusionThe present study found that RAS might induce β-cell dedifferentiation via angiotensin II receptor type 1 activation, which was promoted by NF-κb signaling. Therefore, blocking RAS or NF-kb signaling efficiently reversed the dedifferentiated status of β cells, suggesting a potential therapy for patients with type 2 diabetes.
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