ReviewFrontiers in cell and developmental biology2020
Transforming Growth Factor-Beta1 in Diabetic Kidney Disease.
Review in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 138 citations in OpenAlex.
- Exploring the renoprotective potential of Beta vulgaris in diabetic nephropathy: an integrated network pharmacology, molecular docking and dynamics simulation study.Molecular diversity · 2026Article
- Biomarkers in Diabetic Kidney Disease: Early Detection, Prognostic Assessment, and Integration with Multi-Omics Signatures.Life (Basel, Switzerland) · 2026Review
- AI-guided identification of natural CTSL inhibitors with therapeutic potential for renal injury.PLoS computational biology · 2026Article
- Review
- Advances in targeted treatment of ferroptosis in diabetic kidney disease with SGLT2 inhibitors.Diabetology & metabolic syndrome · 2026Review
- Associations of Socioeconomic Status With Cardiorenal Metabolic Multimorbidity: Evidence From the UK Biobank Cohort.JACC. Advances · 2026Article
- Astragaloside IV: A multipotent phytochemical for treating fibrotic diseases (Review).International journal of molecular medicine · 2026Review
- Potential Mechanisms of Sodium-Glucose Cotransporter 2 Inhibitors in Regulating Cardiac and Renal Fibrosis.Cardiorenal medicine · 2026Review
- TGF-β1 Gene Polymorphisms in Saudi Patients With Type 2 Diabetes With or Without Diabetic Nephropathy.International journal of endocrinology · 2026Article
- Saudi Heart Association Scientific Statement on Cardiovascular-Kidney-Liver-Metabolic (CKLM) Syndrome.Journal of the Saudi Heart Association · 2026Article
- Unveiling the immune microenvironment in diabetic nephropathy: from mechanisms to therapeutics.Frontiers in immunology · 2026Review
- Mechanisms of diabetic kidney disease and established and emerging treatments.Nature reviews. Endocrinology · 2026Review
- Temporal glomerular gene expression dynamics during disease progression in a mouse model of hypertension-accelerated diabetic kidney disease.Animal models and experimental medicine · 2025Article
- TGF-β: elusive target in diabetic kidney disease.Renal failure · 2025Review
- Carvedilol-loaded self-nanoemulsifying drug delivery system target diabetic nephropathy: preclinical evidence of antioxidant and antifibrotic effects.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- The Linkage Between Inflammation and the Progression of Type 2 Diabetes Mellitus.Current issues in molecular biology · 2025Article
- Decoding diabetic kidney disease: a comprehensive review of interconnected pathways, molecular mediators, and therapeutic insights.Diabetology & metabolic syndrome · 2025Review
- NR4A1 silencing alleviates high-glucose-stimulated HK-2 cells pyroptosis and fibrosisWorld journal of diabetes · 2025Article
- Targeting senescence to prevent diabetic kidney disease: Exploring molecular mechanisms and potential therapeutic targets for disease management.Diabetic medicine : a journal of the British Diabetic Association · 2025Review
- Crosstalk between ferroptosis and innate immune in diabetic kidney disease: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
19 more citing papers are in PubMed but not listed here.
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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease (ESRD) worldwide. Renin-angiotensin-aldosterone system (RAAS) inhibitors and sodium-glucose co-transporter 2 (SGLT2) inhibitors have shown efficacy in reducing the risk of ESRD. However, patients vary in their response to RAAS blockades, and the pharmacodynamic responses to SGLT2 inhibitors decline with increasing severity of renal impairment. Thus, effective therapy for DKD is yet unmet. Transforming growth factor-β1 (TGF-β1), expressed by nearly all kidney cell types and infiltrating leukocytes and macrophages, is a pleiotropic cytokine involved in angiogenesis, immunomodulation, and extracellular matrix (ECM) formation. An overactive TGF-β1 signaling pathway has been implicated as a critical profibrotic factor in the progression of chronic kidney disease in human DKD. In animal studies, TGF-β1 neutralizing antibodies and TGF-β1 signaling inhibitors were effective in ameliorating renal fibrosis in DKD. Conversely, a clinical study of TGF-β1 neutralizing antibodies failed to demonstrate renal efficacy in DKD. However, overexpression of latent TGF-β1 led to anti-inflammatory and anti-fibrosis effects in non-DKD. This evidence implied that complete blocking of TGF-β1 signaling abolished its multiple physiological functions, which are highly associated with undesirable adverse events. Ideal strategies for DKD therapy would be either specific and selective inhibition of the profibrotic-related TGF-β1 pathway or blocking conversion of latent TGF-β1 to active TGF-β1.
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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.