ArticleScientific reports2022
Direct evidence of proximal tubular proliferation in early diabetic nephropathy.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Transcriptomics of S3 segment in mice: response to type 1 diabetes, SGLT1/2 inhibition, or GLP1 receptor agonism.American journal of physiology. Renal physiology · 2026Article
- Metabolic reprogramming in diabetes and other endocrine and metabolic disorders: exploring the Warburg effect, ketones, and SGLT2 inhibitors.Reviews in endocrine & metabolic disorders · 2026Review
- Tibia length is an appropriate standard for evaluating hypertrophy in streptozotocin-induced diabetic complications.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Zinc, type 2 diabetes, diabetic kidney disease: focus on hypoxia.Frontiers in endocrinology · 2026Review
- Smurf2 knockdown attenuates the progression of diabetic nephropathy by inhibiting mesangial cell proliferation and fibrosis through suppressing EYA2 ubiquitination.Renal failure · 2025Article
- Injured tubule derived CCN1 exacerbates renal congestion-mediated acute kidney injury and fibrosis.Scientific reports · 2025Article
- Injured tubular epithelia-derived CCN1 promotes the mobilization of fibroblasts toward injury sites after kidney injury.iScience · 2025Article
- Study on effect of pancreatic kininogenase on diabetic nephropathy-induced fibrosis via Notch1/Hes1/Pten/Akt signaling pathway.BMC nephrology · 2025Article
- MiR-192-5p targets cell cycle regulation in diabetic kidney disease via cyclin-dependent kinase inhibitor 3.Non-coding RNA research · 2025Article
- Permanent defects in renal medullary structure and function after reversal of urinary obstruction.JCI insight · 2025Article
- Proximal tubule hypertrophy and hyperfunction: a novel pathophysiological feature in disease states.Clinical kidney journal · 2024Review
- The importance of proinflammatory failed-repair tubular epithelia as a predictor of diabetic kidney disease progression.iScience · 2024Article
- Integrative single-cell characterization of a frugivorous and an insectivorous bat kidney and pancreas.Nature communications · 2024Article
- ELABELA protects against diabetic kidney disease by activating high glucose-inhibited renal tubular autophagy.Journal of biomedical research · 2023Article
- Tubular injury in diabetic kidney disease: molecular mechanisms and potential therapeutic perspectives.Frontiers in endocrinology · 2023Review
- Evaluation of the efficacy ofFrontiers in pharmacology · 2023Article
- Empagliflozin increases kidney weight due to increased cell size in the proximal tubule S3 segment and the collecting duct.Frontiers in pharmacology · 2023Article
- Article
- Early renal structural changes and potential biomarkers in diabetic nephropathy.Frontiers in physiology · 2022Review
- Update on Pathogenesis of Glomerular Hyperfiltration in Early Diabetic Kidney Disease.Frontiers in endocrinology · 2022Review
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
Abstract
Kidney hypertrophy is a common clinical feature in patients with diabetes and is associated with poor renal outcomes. Initial cell proliferation followed by cellular hypertrophy are considered the responsible mechanisms for diabetic kidney hypertrophy. However, whether similar responses against hyperglycemia continue in the chronic phase in diabetes is unclear. We performed lineage tracing analysis of proximal tubular epithelia using novel type 2 diabetic mice with a tamoxifen-inducible proximal tubule-specific fluorescent reporter. Clonal analysis of proximal tubular epithelia demonstrated that the labeled epithelia proliferated in type 2 diabetic mice. Based on the histological analysis and protein/DNA ratio of sorted labeled tubular epithelia, there was no evidence of cellular hypertrophy in type 2 diabetic mice. Lineage tracing and histological analyses of streptozocin-induced type 1 diabetes also revealed that cellular proliferation occurs in the chronic phase of type 1 diabetes induction. According to our study, epithelial proliferation accompanied by SGLT2 upregulation, rather than cellular hypertrophy, predominantly occurs in the hypertrophic kidney in both type 1 and type 2 diabetes. An increased number of SGLT2+ tubular epithelia may be an adaptive response against hyperglycemia, and linked to the hyper-reabsorption of sodium and glucose observed in type 2 diabetes patients.
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