ArticleMolecular and cellular biochemistry2015
The novel role of TRPC6 in vitamin D ameliorating podocyte injury in STZ-induced diabetic rats.
Article in Molecular and cellular biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 62 citations in OpenAlex.
- Relationship of Vitamin-D Deficiency with Kidney Disease in Patients with Type-2 Diabetes Mellitus (T2DM) in the Makkah Region: A Cross-Sectional Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- A Quest for Potential Role of Vitamin D in Type II Diabetes Mellitus Induced Diabetic Kidney Disease.Current pharmaceutical design · 2024Review
- The influence of calcitriol and methylprednisolone on podocytes function in minimal change disease in vitro model.Scientific reports · 2023Article
- Vitamin D deficiency contributes to the diabetic kidney disease progression via increase ZEB1/ZEB2 expressions.Nutrition & diabetes · 2023Article
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- Vitamin D/vitamin D receptor/Atg16L1 axis maintains podocyte autophagy and survival in diabetic kidney disease.Renal failure · 2022Article
- Anti-proteinuria effect of active vitamin D in patients with type 2 diabetic nephropathy.Journal of family medicine and primary care · 2022Article
- The Role of Vitamin D in Diabetic Nephropathy: A Translational Approach.International journal of molecular sciences · 2022Review
- Article
- Research progress on exosomes/microRNAs in the treatment of diabetic retinopathy.Frontiers in endocrinology · 2022Review
- Klotho Ameliorates Podocyte Injury through Targeting TRPC6 Channel in Diabetic Nephropathy.Journal of diabetes research · 2022Article
- Exosomal microRNA-16-5p from human urine-derived stem cells ameliorates diabetic nephropathy through protection of podocyte.Journal of cellular and molecular medicine · 2021Article
- Vitamin D and Glomerulonephritis.Medicina (Kaunas, Lithuania) · 2021Review
- Exosomes: Biomarkers and Therapeutic Targets of Diabetic Vascular Complications.Frontiers in endocrinology · 2021Review
- Vitamin D/VDR Protects Against Diabetic Kidney Disease by Restoring Podocytes Autophagy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- The Wnt Signaling Pathway in Diabetic Nephropathy.Frontiers in cell and developmental biology · 2021Review
- The Emerging Role of Vitamin D and Vitamin D Receptor in Diabetic Nephropathy.BioMed research international · 2020Review
- TRPC Channels in Proteinuric Kidney Diseases.Cells · 2019Review
- TRPC6 inactivation does not protect against diabetic kidney disease in streptozotocin (STZ)-treated Sprague-Dawley rats.FASEB bioAdvances · 2019Article
- Knockout of TRPC6 promotes insulin resistance and exacerbates glomerular injury in Akita mice.Kidney international · 2019Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Podocyte injury plays a critical role in the development and progression of diabetic nephropathy (DN). Over expression of TRPC6 on the podocytes has been revealed to cause podocyte injury in non-diabetic states. Besides, the emerging evidence from clinic revealed that vitamin D could reduce albuminuria and improve renal function, which was associated with podocyte protection. Our study aimed to investigate whether calcitriol ameliorating podocyte impairment is associated with regulation of the expression of TRPC6 in STZ-induced rats. Sprague-Dawley rats were randomly divided into three groups: normal control, DN, and DN treated with calcitriol (DN + VD); VD rats were treated with 0.1 μg/kg/d calcitriol by gavage. DN model rats were established by intraperitoneal injections of streptozocin. The rats were sacrificed after 18 weeks treatment. DN rats exhibited increased proteinuria accompanied by elevated TRPC6 expression. Treatment with calcitriol not only reduced proteinuria, but also normalized TRPC6 expression. Meanwhile, in DN rats, the expression of podocyte specific markers including nephrin and podocin was significantly decreased, accompanied by increased desmin, a marker of podocyte injury. Treatment with calcitriol reversed above changes. In addition, vitamin D receptor (VDR) was significantly decreased, whereas this reduction was attenuated by the calcitriol treatment. Moreover, TRPC6 was positively correlated with both 24 h urinary protein and desmin. In contrast, TRPC6 was negatively correlated with both VDR and nephrin expression in podocytes. Calcitriol can ameliorate podocyte injury, which is contributed by the inhibition of enhanced TRPC6 expression in the early stages of DN rats.
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