ArticleJCI insight2019
Alteration of thyroid hormone signaling triggers the diabetes-induced pathological growth, remodeling, and dedifferentiation of podocytes.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 33 citations in OpenAlex.
- Correlations Among Glycemia and Glucose Variability, Thyroid Hormones, and Albuminuria in Patients With Type 2 Diabetes Mellitus.The Kaohsiung journal of medical sciences · 2026Article
- The abnormal thyroxine signals triggers podocyte apoptosis in DN mice.In vitro cellular & developmental biology. Animal · 2026Article
- Thyroid Hormone Indices and Histopathological Severity of Diabetic Nephropathy in Euthyroid Patients with Type 2 Diabetes: A Biopsy-Based Cross-Sectional Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Association Between Thyroid Hormone Levels with Diabetic Kidney Disease Among Euthyroid Participants with Type 2 Diabetes Mellitus: A Cross-Sectional Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Cell cycle disorders in podocytes: an emerging and increasingly recognized phenomenon.Cell death discovery · 2025Review
- METTL10 attenuates adriamycin-induced podocyte injury by targeting cell dedifferentiation.Scientific reports · 2025Article
- Losartan is more effective than angiotensin (1-7) in preventing thyroxine-induced renal injury in the rat.Thyroid research · 2024Article
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- The predictive value of free thyroxine combined with tubular atrophy/interstitial fibrosis for poor prognosis in patients with IgA nephropathy.Frontiers in endocrinology · 2024Article
- Impaired Sensitivity to Thyroid Hormones is Associated with the Risk of Diabetic Nephropathy in Euthyroid Patients with Type 1 Diabetes Mellitus.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- Thyroid hormone treatment counteracts cellular phenotypical remodeling in diabetic organs.iScience · 2023Article
- Free triiodothyronine predicts the risk of developing diabetic kidney disease.BMC nephrology · 2023Article
- Minimal change disease with papillary thyroid carcinoma: a report of two adult cases.BMC nephrology · 2023Article
- Association between thyroid hormones and diabetic kidney disease in Chinese adults.BMC endocrine disorders · 2023Article
- Editorial: Endocrine abnormalities and renal complications.Frontiers in endocrinology · 2023Article
- Advance in the Correlation between Diabetic Nephropathy and Abnormal Serum Thyroid Hormone Levels in Patients.Emergency medicine international · 2023Article
- The analysis of risk factors for diabetic kidney disease progression: a single-centre and cross-sectional experiment in Shanghai.BMJ open · 2022Article
- Yishen Capsule Alleviated Symptoms of Diabetic Nephropathy via NOD-like Receptor Signaling Pathway.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Article
- Cell Hypertrophy: A "Biophysical Roadblock" to Reversing Kidney Injury.Frontiers in cell and developmental biology · 2022Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thyroid hormone (TH) signaling is a universal regulator of metabolism, growth, and development. Here, we show that TH-TH receptor (TH-TR) axis alterations are critically involved in diabetic nephropathy-associated (DN-associated) podocyte pathology, and we identify TRα1 as a key regulator of the pathogenesis of DN. In ZSF1 diabetic rats, T3 levels progressively decreased during DN, and this was inversely correlated with metabolic and renal disease worsening. These phenomena were associated with the reexpression of the fetal isoform TRα1 in podocytes and parietal cells of both rats and patients with DN and with the increased glomerular expression of the TH-inactivating enzyme deiodinase 3 (DIO3). In diabetic rats, TRα1-positive cells also reexpressed several fetal mesenchymal and damage-related podocyte markers, while glomerular and podocyte hypertrophy was evident. In vitro, exposing human podocytes to diabetes milieu typical components markedly increased TRα1 and DIO3 expression and induced cytoskeleton rearrangements, adult podocyte marker downregulation and fetal kidney marker upregulation, the maladaptive cell cycle induction/arrest, and TRα1-ERK1/2-mediated hypertrophy. Strikingly, T3 treatment reduced TRα1 and DIO3 expression and completely reversed all these alterations. Our data show that diabetic stress induces the TH-TRα1 axis to adopt a fetal ligand/receptor relationship pattern that triggers the recapitulation of the fetal podocyte phenotype and subsequent pathological alterations.
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