ReviewCurrent hypertension reports2019
Role of TRPC6 in Progression of Diabetic Kidney Disease.
Review in Current hypertension reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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
44 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Focus on podocytes: diabetic kidney disease and renal fibrosis - a global bibliometric analysis (2000-2024).Frontiers in pharmacology · 2024Pooled it
- Transient receptor potential canonical (TRPC) channels in diabetes and associated complications.Channels (Austin, Tex.) · 2026Review
- Urotensin II Receptor Deletion Mitigates Kidney Injury and Renal Lipid Remodeling in Mice Fed a Long-Term High-Fat Diet.FASEB bioAdvances · 2026Article
- TRPC6 governs brown adipose thermogenesis via a BMPR2-p38 MAPK signaling axis.Molecular metabolism · 2026Article
- Physiological functions and pharmacological targeting of transient receptor potential channels.Pharmacological reviews · 2025Review
- Mechanosensing of Shear Stress and Uterine Spiral Artery Remodeling by Invasive Trophoblasts in Early Pregnancy.International journal of molecular sciences · 2025Review
- The CaPediatric nephrology (Berlin, Germany) · 2025Review
- Targeting REDD1 in Podocytes: A Promising Strategy for Mitigating Diabetic Kidney Injury.Diabetes · 2025Article
- Podocyte-Specific Expression of the Stress Response Protein REDD1 Is Necessary for Diabetes-Induced Podocytopenia.Diabetes · 2025Article
- TRPC6-Calpain-1 Axis Promotes Tubulointerstitial Inflammation by Inhibiting Mitophagy in Diabetic Kidney Disease.Kidney international reports · 2024Article
- Non-voltage-gated CaAmerican journal of physiology. Renal physiology · 2024Review
- Article
- Comprehensive strategy for identifying extracellular vesicle surface proteins as biomarkers for chronic kidney disease.Frontiers in physiology · 2024Review
- A Putative Role for TRPC6 in Immune-Mediated Kidney Injury.International journal of molecular sciences · 2023Review
- Role of Neuronal TRPC6 Channels in Synapse Development, Memory Formation and Animal Behavior.International journal of molecular sciences · 2023Review
- An inactivating human TRPC6 channel mutation without focal segmental glomerulosclerosis.Cellular and molecular life sciences : CMLS · 2023Article
- Transient Receptor Potential Canonical 6 (TRPC6) Channel in the Pathogenesis of Diseases: A Jack of Many Trades.Inflammation · 2023Review
- TRP (transient receptor potential) ion channel family: structures, biological functions and therapeutic interventions for diseases.Signal transduction and targeted therapy · 2023Review
- Reorganization and Suppression of Store-Operated Calcium Entry in Podocytes of Type 2 Diabetic Rats.International journal of molecular sciences · 2023Article
- 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
3 authors.
Funding
Abstract
purpose of reviewThe underlining goal of this review is to offer a concise, detailed look into current knowledge surrounding transient receptor potential canonical channel 6 (TRPC6) in the progression of diabetic kidney disease (DKD). RECENT
findingsMutations and over-activation in TRPC6 channel activity lead to the development of glomeruli injury. Angiotensin II, reactive oxygen species, and other factors in the setting of DKD stimulate drastic increases in calcium influx through the TRPC6 channel, causing podocyte hypertrophy and foot process effacement. Loss of the podocytes further promote deterioration of the glomerular filtration barrier and play a major role in the development of both albuminuria and the renal injury in DKD. Recent genetic manipulation with TRPC6 channels in various rodent models provide additional knowledge about the role of TRPC6 in DKD and are reviewed here. The TRPC6 channel has a pronounced role in the progression of DKD, with deviations in activity yielding detrimental outcomes. The benefits of targeting TRPC6 or its upstream or downstream signaling pathways in DKD are prominent.
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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.