ArticleAmerican journal of physiology. Renal physiology2018
Adiponectin attenuates kidney injury and fibrosis in deoxycorticosterone acetate-salt and angiotensin II-induced CKD mice.
Article in American journal of physiology. Renal physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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21 citing papers in PubMed, 35 citations in OpenAlex.
- Review
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- The functional role of the extracellular matrix in inflammatory bowel disease associated gut fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2025Review
- RNA-binding protein HuR regulates the transition of septic AKI to CKD by modulating CD147.Clinical science (London, England : 1979) · 2025Article
- Repurposing Niclosamide to Modulate Renal RNA-Binding Protein HuR for the Treatment of Diabetic Nephropathy in db/db Mice.International journal of molecular sciences · 2024Article
- The mysterious association between adiponectin and endometriosis.Frontiers in pharmacology · 2024Review
- Targeting RNA-binding protein HuR to inhibit the progression of renal tubular fibrosis.Journal of translational medicine · 2023Article
- Adrenomedullin Mitigates Doxorubicin-Induced Nephrotoxicity in Rats: Role of Oxidative Stress, Inflammation, Apoptosis, and Pyroptosis.International journal of molecular sciences · 2022Article
- Ceramides and Acute Kidney Injury.Seminars in nephrology · 2022Review
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- Lipid Disorders in NAFLD and Chronic Kidney Disease.Biomedicines · 2021Review
- Key role for EphB2 receptor in kidney fibrosis.Clinical science (London, England : 1979) · 2021Article
- The Potential of Albuminuria as a Biomarker of Diabetic Complications.Cardiovascular drugs and therapy · 2021Review
- From diabetes to renal aging: the therapeutic potential of adiponectin.Journal of physiology and biochemistry · 2021Review
- Adiponectin Modified BMSCs Alleviate Heart Fibrosis via Inhibition TGF-beta1/Smad in Diabetic Rats.Frontiers in cell and developmental biology · 2021Article
- Association of High Serum Adiponectin Level With Adverse Cardiovascular Outcomes and Progression of Coronary Artery Calcification in Patients With Pre-dialysis Chronic Kidney Disease.Frontiers in cardiovascular medicine · 2021Article
- Combined donor-recipient genotypes of leptin receptor and adiponectin gene polymorphisms affect the incidence of complications after renal transplantation.Molecular genetics and metabolism reports · 2020Article
- Adipocytes protect fibroblasts from radiation-induced damage by adiponectin secretion.Scientific reports · 2020Article
- Association of polymorphisms in leptin and adiponectin genes with long-term outcomes in renal transplant recipients.The pharmacogenomics journal · 2020Article
- Adiponectin in renal fibrosis.Aging · 2020Review
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5 authors at 3 institutions in 2 countries.
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Abstract
Adiponectin (ApN) is a multifunctional adipokine. However, high, rather than low, concentrations of ApN are unexpectedly found in patients with chronic kidney disease (CKD) via an as yet unknown mechanism, and the role of ApN in CKD is unclear. Herein, we investigated the effect of ApN overexpression on progressive renal injury resulting from deoxycorticosterone acetate-salt (DOCA) and angiotensin II (ANG II) infusion using a transgenic, inducible ApN-overexpressing mouse model. Three groups of mice [wild type receiving no infusion (WT) and WT and cytochrome P450 1a1 (cyp1a1)-ApN transgenic mice (ApN-Tg) receiving DOCA+ANG II infusion (WT/DOCA+ANG II and ApN-Tg/DOCA+ANG II)] were assigned to receive normal food containing 0.15% of the transgene inducer indole-3-carbinol (I3C) for 3 wk. In the I3C-induced ApN-Tg/DOCA+ANG II mice, not the WT or WT/DOCA+ANG II mice, overexpression of ApN in liver resulted in 3.15-fold increases in circulating ApN compared with nontransgenic controls. Of note, the transgenic mice receiving DOCA+ANG II infusion were still hypertensive but had much less albuminuria and glomerular and tubulointerstitial fibrosis, which were associated with ameliorated podocyte injury determined by ameliorated podocyte loss and foot process effacement, and alleviated tubular injury determined by ameliorated mRNA overexpression of kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin and mRNA decreases of cubilin and megalin in tubular cells, compared with WT/DOCA+ANG II mice. In addition, renal production of NF-κB-p65, NAPDH oxidase 2, and p47
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