ArticleJournal of nephrology2016
Adiponectin secreted by tubular renal cells during LPS exposure worsens the cellular inflammatory damage.
Article in Journal of nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Adipokine networks in diabetic kidney disease: mechanistic insights and therapeutic implications.Lipids in health and disease · 2026Review
- Endogenous renal adiponectin drives gluconeogenesis through enhancing pyruvate and fatty acid utilization.Nature communications · 2023Article
- Prognostic value of metabolic syndrome in renal structural changes in type 2 diabetes.International urology and nephrology · 2022Article
- Adiponectin in renal fibrosis.Aging · 2020Review
- ZFP36L1 and AUF1 Induction Contribute to the Suppression of Inflammatory Mediators Expression by Globular Adiponectin via Autophagy Induction in Macrophages.Biomolecules & therapeutics · 2018Article
- Assessment of physical performance and body composition in male renal transplant patients.Journal of nephrology · 2018Article
- Uric acid upregulates the adiponectin‑adiponectin receptor 1 pathway in renal proximal tubule epithelial cells.Molecular medicine reports · 2018Article
- Immunologic and endocrine functions of adipose tissue: implications for kidney disease.Nature reviews. Nephrology · 2018Review
- Ultrapure dialysis water obtained with additional ultrafilter may reduce inflammation in patients on hemodialysis.Journal of nephrology · 2017Article
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
The pathogenetic role of adiponectin (ADPN) in kidney failure is not yet elucidated, since in vitro and in vivo studies have demonstrated that ADPN exerts both anti-inflammatory and pro-inflammatory effects. Starting from our previous findings demonstrating that HK-2 cells express and secrete ADPN, in this study we investigated the autocrine role of ADPN in tubular inflammatory damage induced by lipopolysaccharide (LPS) and the underlying molecular mechanisms. Firstly, we observed that short-term exposure to LPS enhanced ADPN protein expression as well as the adiponectin receptor ADIPOR1 mRNA content together with its signaling pathway downstream, pAMPK/pERK/pJNK, whose up-regulation status was reversed when ADPN gene knockdown occurred. Interestingly, in the same experimental conditions, we observed that ADPN mediated the nuclear translocation of the transcription factors nuclear factor kappa B (NFkB) and pcFos/pcJun (activator protein 1, AP-1), both induced by the pJNK pathway and involved in tumor necrosis factor (TNF)-α transactivation. Indeed, by transient transfection assay, we observed that the LPS-induced increase of TNF-α promoter activity was abrogated in cells pretreated with the inhibitors of NFkB and AP-1. Collectively our results suggest that in HK-2 cells, ADPN produced upon LPS stimulus could worsen the inflammatory damage in an autocrine-dependent manner.
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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.