ArticleJournal of the American Society of Nephrology : JASN2008
Rap1b GTPase ameliorates glucose-induced mitochondrial dysfunction.
Article in Journal of the American Society of Nephrology : JASN, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 77 citations in OpenAlex.
- Role of MIR-101-3P/RAP1B Axis and Insulin Protection in Glucose-Induced Stress in HK-2 Cell Model for Diabetic Kidney Disease.Cell biochemistry and biophysics · 2026Article
- Targeting METTL16 attenuates mesangial cell viability and fibrosis in a high-glucose state by suppressing m6A modification and the expression of RAP1B.BMC molecular and cell biology · 2025Article
- The Role of Mitochondria in Diabetic Kidney Disease and Potential Therapeutic Targets.Kidney international reports · 2025Review
- Metallo-protease Peptidase M84 fromiScience · 2024Article
- The potential mechanism of gut microbiota-microbial metabolites-mitochondrial axis in progression of diabetic kidney disease.Molecular medicine (Cambridge, Mass.) · 2023Review
- Carnosine alleviates kidney tubular epithelial injury by targeting NRF2 mediated ferroptosis in diabetic nephropathy.Amino acids · 2023Article
- Upregulation of TIPE1 in tubular epithelial cell aggravates diabetic nephropathy by disrupting PHB2 mediated mitophagy.Redox biology · 2022Article
- CX3CL1 Worsens Cardiorenal Dysfunction and Serves as a Therapeutic Target of Canagliflozin for Cardiorenal Syndrome.Frontiers in pharmacology · 2022Article
- Homoarginine ameliorates diabetic nephropathy independent of nitric oxide synthase-3.Physiological reports · 2021Article
- Selective inhibition of arginase-2 in endothelial cells but not proximal tubules reduces renal fibrosis.JCI insight · 2020Article
- ORP8 induces apoptosis by releasing cytochrome c from mitochondria in non‑small cell lung cancer.Oncology reports · 2020Article
- High glucose induces phosphorylation and oxidation of mitochondrial proteins in renal tubular cells: A proteomics approach.Scientific reports · 2020Article
- The Role of PGC-1α and Mitochondrial Biogenesis in Kidney Diseases.Biomolecules · 2020Review
- Mitochondria-Associated Endoplasmic Reticulum Membranes (MAMs) and Their Prospective Roles in Kidney Disease.Oxidative medicine and cellular longevity · 2020Review
- Mitochondrial Dysfunction in the Transition from NASH to HCC.Metabolites · 2019Review
- Huangqi-Danshen Decoction Ameliorates Adenine-Induced Chronic Kidney Disease by Modulating Mitochondrial Dynamics.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Chloroquine and amodiaquine enhance AMPK phosphorylation and improve mitochondrial fragmentation in diabetic tubulopathy.Scientific reports · 2018Article
- Reactive oxygen species promote tubular injury in diabetic nephropathy: The role of the mitochondrial ros-txnip-nlrp3 biological axis.Redox biology · 2018Article
- Mitochondrial dysfunction in diabetic kidney disease.Nature reviews. Nephrology · 2018Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 8 institutions in 4 countries.
Funding
Abstract
The role of tubular injury in diabetic nephropathy is relatively unknown, despite that apoptosis of tubular epithelial cells is commonly observed in human renal biopsies. The GTPase Ras-proximate-1 (Rap1b) is upregulated in the hyperglycemic state and is known to increase B-Raf, an antiapoptotic effector protein. In this study, the effects of high glucose on renal tubular apoptosis and the potential ability for Rap1b to ameliorate these effects were investigated. In the kidneys of diabetic mice, apoptotic tubular cells and dysmorphic mitochondria were observed, Bcl-2 expression was decreased, and Bax expression was increased. Total Rap1b expression was slightly increased, but its associated GTPase activity was significantly decreased. In vitro, high extracellular glucose led to decreased Bcl-2 expression, reduced Rap1b GTPase activity, and increased levels of both Bax and GTPase activating protein in a proximal tubular cell line (HK-2). These changes were accompanied by increased DNA fragmentation, decreased high molecular weight mitochondrial DNA, altered mitochondrial morphology and function, disrupted Bcl-2-Bax and Bcl-2-Rap1b interactions, and reduced cell survival. Overexpression of Rap1b partially prevents these abnormalities. Furthermore, the BH4 domain of Bcl-2 was found to be required for successful protein-protein interaction between Bcl-2 and Rap1b. In summary, these data suggest that Rap1b ameliorates glucose-induced mitochondrial dysfunction in renal tubular cells.
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.