ArticleScientific reports2023
Periostin deficiency attenuates kidney fibrosis in diabetic nephropathy by improving pancreatic β-cell dysfunction and reducing kidney EMT.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Urinary periostin as a novel non-invasive biomarker for kidney scarring in pediatric vesicoureteral reflux patients.Pediatric nephrology (Berlin, Germany) · 2026Article
- SMOC2 promotes partial epithelial-mesenchymal transition and maladaptive repair in renal tubular epithelial cells.JCI insight · 2026Article
- Molecular mechanisms, therapeutic strategies, and inter-organ fibrosis crosstalk of Gla proteins in cardiovascular disease.Communications biology · 2026Review
- Hepatocyte growth factor blocks epithelial-mesenchymal transition and fibrosis of ureteral epithelial cells in UPJO.BMC pediatrics · 2026Article
- Targeting Cardiac Fibroblast Plasticity for Antifibrotic and Regenerative Therapy in Heart Failure.Cells · 2026Review
- Translational advances in diabetic nephropathy management: integrating nanoformulation-based drug delivery systems.Frontiers in medical technology · 2026Review
- CD248, targeted by veratramine and neobavaisoflavone, mediates pathological changes of renal tubular epithelial cells induced by high glucose.Hereditas · 2025Article
- Role of serum periostin level as profibrotic marker in conjunction with renal resistivity index and shear wave elastography in predicting renal fibrosis in diabetic nephropathy.BMC nephrology · 2025Article
- O-linked β-N-acetylglucosamine (O-GlcNAc) modification: Emerging pathogenesis and a therapeutic target of diabetic nephropathy.Diabetic medicine : a journal of the British Diabetic Association · 2025Review
- Periostin Induces Epithelial-Mesenchymal Transition via p38-MAPK Pathway in Human Renal Tubular Cells by High Glucose.Immunity, inflammation and disease · 2024Article
- Comprehensive ultrasonographic evaluation of normal and fibrotic kidneys in a mouse model with an ultra-high-frequency transducer.Ultrasonography (Seoul, Korea) · 2024Article
- Renal Fibrosis: SIRT1 Still of Value.Biomedicines · 2024Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) is associated with kidney fibrosis. A previous study revealed that periostin (POSTN) contributes to kidney fibrosis. This study examined the role of POSTN in DN. The urinary concentrations of POSTN and TNC increased according to the severity of DN in human samples. Streptozotocin (STZ) was administered after unilateral nephrectomy (UNXSTZ) to induce DN in wild-type and Postn-null mice. Four experimental groups were generated: wild-typeham (WT Sham), wild-type UNXSTZ (WT STZ), Postn-null Sham (KO Sham), and Postn-null UNXSTZ (KO STZ). After 20 weeks, the KO STZ group had lower levels of urine albumin excretion, glomerular sclerosis, and interstitial fibrosis than those of the WT STZ group. Additionally, the KO STZ group had lower expression of fibrosis markers, including TNC. The KO STZ group showed better glucose regulation than the WT STZ model. Furthermore, the KO STZ group exhibited significantly preserved pancreatic islet integrity and insulin expression. HK-2 cells were used to observe the aggravation of fibrosis caused by POSTN under TGF-β conditions. We stimulated INS-1 cells with streptozotocin and evaluated the viability of these cells. The anti-POSTN antibody treatment of INS-1 cells with streptozotocin resulted in higher cell viability than that with treatment with streptozotocin alone. The absence of POSTN in DN contributes to renal fibrosis alleviation by improving pancreatic β-cell function. Additionally, there is an association between POSTN and TNC.
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