ArticleScientific reports2016
Effect of Antifibrotic MicroRNAs Crosstalk on the Action of N-acetyl-seryl-aspartyl-lysyl-proline in Diabetes-related Kidney Fibrosis.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 66 citations in OpenAlex.
- Kidney angiopoietin-like protein 4 regulates fibrotic responses in diabetic kidney disease.Frontiers in pharmacology · 2026Review
- The Role of Sirt3 in Kidney Health and Disease.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The molecular determinants regulating redox signaling in diabetic endothelial cells.Frontiers in pharmacology · 2025Review
- Renal Angptl4 is a key fibrogenic molecule in progressive diabetic kidney disease.Science advances · 2024Article
- HOXD10 attenuates renal fibrosis by inhibiting NOX4-induced ferroptosis.Cell death & disease · 2024Article
- Urinary miR-185-5p is a biomarker of renal tubulointerstitial fibrosis in IgA nephropathy.Frontiers in immunology · 2024Article
- Drugs for Diabetes: From Pharmacology to Clinical Application.Pharmaceuticals (Basel, Switzerland) · 2023Article
- RAGE signaling regulates the progression of diabetic complications.Frontiers in pharmacology · 2023Review
- Therapeutic potential of urine exosomes derived from rats with diabetic kidney disease.Frontiers in endocrinology · 2023Article
- YY1-induced upregulation of LncRNA-ARAP1-AS2 and ARAP1 promotes diabetic kidney fibrosisFrontiers in pharmacology · 2023Article
- Editorial: Current understanding of complications associated with diabetes.Frontiers in clinical diabetes and healthcare · 2023Article
- Editorial: Receptor biology and cell signaling in diabetes: volume II.Frontiers in pharmacology · 2023Article
- Editorial: Diabetic kidney disease: routes to drug development, pharmacology and underlying molecular mechanisms.Frontiers in pharmacology · 2023Article
- Epigenetic modification in diabetic kidney disease.Frontiers in endocrinology · 2023Review
- The Role of Tβ4-POP-Ac-SDKP Axis in Organ Fibrosis.International journal of molecular sciences · 2022Review
- MicroRNAs in kidney injury and disease.Nature reviews. Nephrology · 2022Review
- Research progress of endothelial-mesenchymal transition in diabetic kidney disease.Journal of cellular and molecular medicine · 2022Review
- circSTRN3 aggravates sepsis-induced acute kidney injury by regulating miR-578/ toll like receptor 4 axis.Bioengineered · 2022Article
- Editorial: Receptor Biology and Cell Signaling in Diabetes.Frontiers in pharmacology · 2022Article
- MicroRNA miR-4709-3p targets Large Tumor Suppressor Kinase 2 (LATS2) and induces obstructive renal fibrosis through Hippo signaling.Bioengineered · 2021Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) is an endogenous antifibrotic peptide. We found that suppression of AcSDKP and induction of dipeptidyl peptidase-4 (DPP-4), which is associated with insufficient levels of antifibrotic microRNA (miR)s in kidneys, were imperative to understand the mechanisms of fibrosis in the diabetic kidneys. Analyzing streptozotocin (STZ)-induced diabetic mouse strains, diabetic CD-1 mice with fibrotic kidneys could be differentiated from less-fibrotic diabetic 129Sv mice by suppressing AcSDKP and antifibrotic miRs (miR-29s and miR-let-7s), as well as by the prominent induction of DPP-4 protein expression/activity and endothelial to mesenchymal transition. In diabetic CD-1 mice, these alterations were all reversed by AcSDKP treatment. Transfection studies in culture endothelial cells demonstrated crosstalk regulation of miR-29s and miR-let-7s against mesenchymal activation program; such bidirectional regulation could play an essential role in maintaining the antifibrotic program of AcSDKP. Finally, we observed that AcSDKP suppression in fibrotic mice was associated with induction of both interferon-γ and transforming growth factor-β signaling, crucial molecular pathways that disrupt antifibrotic miRs crosstalk. The present study provides insight into the physiologically relevant antifibrotic actions of AcSDKP via antifibrotic miRs; restoring such antifibrotic programs could demonstrate potential utility in combating kidney fibrosis in diabetes.
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