ReviewFrontiers of medicine2017
Non-genetic mechanisms of diabetic nephropathy.
Review in Frontiers of medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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.
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.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Pooled it
- Circulating Lymphocyte Subsets Are Associated with Diabetic Kidney Disease and Overall Survival in Patients with Type 2 Diabetes.Biomedicines · 2026Article
- AARS1-mediated lactylation of H3K18 and STAT1 promotes ferroptosis in diabetic nephropathy.Cell death and differentiation · 2026Article
- DOTAP-Based Hybrid Nanostructured Lipid Carriers for CRISPR-Cas9 RNP Delivery TargetingPharmaceutics · 2026Article
- Uncovering the mechanism of Huangkui capsule in the treatment of diabetic kidney disease based on network pharmacology and experimental validation.Scientific reports · 2025Article
- Type 2 Diabetes Mellitus: New Pathogenetic Mechanisms, Treatment and the Most Important Complications.International journal of molecular sciences · 2025Review
- An update on renal tubular injury as related to glycolipid metabolism in diabetic kidney disease.Frontiers in pharmacology · 2025Review
- Hypertension and BMI as Mediators of Type 2 Diabetes-Induced CKD: Insights from an Integrative Multi-Database Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- S1R mediates NRF2 dependent ferroptosis of renal tubular epithelial cells to promote renal fibrosis in diabetic nephropathy.International journal of medical sciences · 2025Article
- The PRMT6/STAT1/ACSL1 axis promotes ferroptosis in diabetic nephropathy.Cell death and differentiation · 2024Article
- Recent Advances in the Management of Diabetic Kidney Disease: Slowing Progression.International journal of molecular sciences · 2024Review
- Identification and validation of voltage-dependent anion channel 1-related genes and immune cell infiltration in diabetic nephropathy.Journal of diabetes investigation · 2024Article
- What's New in the Molecular Mechanisms of Diabetic Kidney Disease: Recent Advances.International journal of molecular sciences · 2022Review
- LncRNA NEAT1/microRNA-124 regulates cell viability, inflammation and fibrosis in high-glucose-treated mesangial cells.Experimental and therapeutic medicine · 2022Article
- Upregulation of TIPE1 in tubular epithelial cell aggravates diabetic nephropathy by disrupting PHB2 mediated mitophagy.Redox biology · 2022Article
- The role of protein kinase C in diabetic microvascular complications.Frontiers in endocrinology · 2022Review
- TNF-α and IL-1β Promote Renal Podocyte Injury in T2DM Rats by Decreasing Glomerular VEGF/eNOS Expression Levels and Altering Hemodynamic Parameters.Journal of inflammation research · 2022Article
- KIAA0101 and IL2RA Were Identified as Core Genes in Hormone-Resistant Nephropathy.Disease markers · 2022Article
- Impact of Diabetic Nephropathy on Pulmonary Function and Clinical Outcomes.Computational intelligence and neuroscience · 2022Article
- Mitochondria in Diabetic Kidney Disease.Cells · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) is one of the most common microvascular complications in diabetes mellitus patients and is characterized by thickened glomerular basement membrane, increased extracellular matrix formation, and podocyte loss. These phenomena lead to proteinuria and altered glomerular filtration rate, that is, the rate initially increases but progressively decreases. DN has become the leading cause of end-stage renal disease. Its prevalence shows a rapid growth trend and causes heavy social and economic burden in many countries. However, this disease is multifactorial, and its mechanism is poorly understood due to the complex pathogenesis of DN. In this review, we highlight the new molecular insights about the pathogenesis of DN from the aspects of immune inflammation response, epithelial-mesenchymal transition, apoptosis and mitochondrial damage, epigenetics, and podocyte-endothelial communication. This work offers groundwork for understanding the initiation and progression of DN, as well as provides ideas for developing new prevention and treatment measures.
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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.