ArticleScientific reports2015
ATP synthase subunit-β down-regulation aggravates diabetic nephropathy.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Advances in Targeting the AGEs-RAGE Pathway for the Treatment of Diabetic Kidney Disease.Drug design, development and therapy · 2026Review
- ATP deficiency triggers ganoderic acids accumulation via fatty acid β-oxidation pathway in Ganoderma lucidum.Microbial cell factories · 2025Article
- High glucose affects the cardiac function of diabetic Akita mice by inhibiting cardiac ATP synthase beta subunit.International journal of cardiology. Cardiovascular risk and prevention · 2025Article
- Establishing protein expression profiles involved in tooth development using a proteomic approach.Odontology · 2023Article
- Transcriptional profiling of matched patient biopsies clarifies molecular determinants of enzalutamide-induced lineage plasticity.Nature communications · 2022Article
- SILAC-based quantitative proteomics to investigate the eicosanoid associated inflammatory response in activated macrophages.Journal of inflammation (London, England) · 2022Article
- Article
- Comprehensive metabolomic study of the response of HK-2 cells to hyperglycemic hypoxic diabetic-like milieu.Scientific reports · 2021Article
- Characterisation of the Myocardial Mitochondria Structural and Functional Phenotype in a Murine Model of Diabetic Cardiomyopathy.Frontiers in physiology · 2021Article
- Comparative proteomic analysis of renal proteins from IgA nephropathy model mice and control mice.Clinical and experimental nephrology · 2020Article
- Blood co-expression modules identify potential modifier genes of diabetes and lung function in cystic fibrosis.PloS one · 2020Article
- Time-series proteomic study of the response of HK-2 cells to hyperglycemic, hypoxic diabetic-like milieu.PloS one · 2020Article
- Article
- Epigenetic Modification of MicroRNA-200b Contributes to Diabetic Vasculopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2017Article
- Mitochondrial HDiabetologia · 2017Article
- The impact of growth hormone on proteomic profiles: a review of mouse and adult human studies.Clinical proteomics · 2017Review
- Involvement of Endoplasmic Reticulum Stress, Autophagy, and Apoptosis in Advanced Glycation End Products-Induced Glomerular Mesangial Cell Injury.Scientific reports · 2016Article
- The pathological role of advanced glycation end products-downregulated heat shock protein 60 in islet β-cell hypertrophy and dysfunction.Oncotarget · 2016Article
- Investigating the Role of EPA and DHA on Cellular Oxidative Stress; Profiling Antidiabetic and Antihypertensive Potential.Journal of pharmacy & bioallied sciencesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we investigated the role of ATP synthase subunit-β (ATP5b) in diabetic nephropathy. Histopathological changes, fibrosis, and protein expressions of α-smooth muscle actin (α-SMA), advanced glycation end-products (AGEs), and ATP5b were obviously observed in the kidneys of db/db diabetic mice as compared with the control db/m(+) mice. The increased ATP5b expression was majorly observed in diabetic renal tubules and was notably observed to locate in cytoplasm of tubule cells, but no significant increase of ATP5b in diabetic glomeruli. AGEs significantly increased protein expression of ATP5b and fibrotic factors and decreased ATP content in cultured renal tubular cells via an AGEs-receptor for AGEs (RAGE) axis pathway. Oxidative stress was also induced in diabetic kidneys and AGEs-treated renal tubular cells. The increase of ATP5b and CTGF protein expression in AGEs-treated renal tubular cells was reversed by antioxidant N-acetylcysteine. ATP5b-siRNA transfection augmented the increased protein expression of α-SMA and CTGF and CTGF promoter activity in AGEs-treated renal tubular cells. The in vivo ATP5b-siRNA delivery significantly enhanced renal fibrosis and serum creatinine in db/db mice with ATP5b down-regulation. These findings suggest that increased ATP5b plays an important adaptive or protective role in decreasing the rate of AGEs-induced renal fibrosis during diabetic condition.
Indexed as
Identifiers
What OpenQuestion holds
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.