ArticleJournal of cellular and molecular medicine2018
The classic signalling and trans-signalling of interleukin-6 are both injurious in podocyte under high glucose exposure.
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
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- Regulation of Renal Transporters by Pro-inflammatory Cytokines in Human Proximal Tubular Epithelial Cells: Identification of the Perpetrator and Mechanisms.bioRxiv : the preprint server for biology · 2025Article
- Crosstalk between ferroptosis and innate immune in diabetic kidney disease: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Targeting inerleukin-6 for renoprotection.Frontiers in immunology · 2024Review
- IL-6 and diabetic kidney disease.Frontiers in immunology · 2024Review
- Recent advances in anti-inflammatory active components and action mechanisms of natural medicines.Inflammopharmacology · 2023Review
- Asparagine endopeptidase protects podocytes in adriamycin-induced nephropathy by regulating actin dynamics through cleaving transgelin.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- NETosis: an emerging therapeutic target in renal diseases.Frontiers in immunology · 2023Review
- JAK/STAT signaling in diabetic kidney disease.Frontiers in cell and developmental biology · 2023Review
- Regulation Networks of Non-Coding RNA-Associated ceRNAs in Cisplatin-Induced Acute Kidney Injury.Cells · 2022Article
- Glomerular cell cross talk in diabetic kidney diseases.Journal of diabetes · 2022Review
- Asparaginyl endopeptidase protects against podocyte injury in diabetic nephropathy through cleaving cofilin-1.Cell death & disease · 2022Article
- MAD2B promotes podocyte injury through regulating Numb-dependent Notch 1 pathway in diabetic nephropathy.International journal of biological sciences · 2022Article
- Regulation of Podocyte Injury by CircHIPK3/FUS Complex in Diabetic Kidney Disease.International journal of biological sciences · 2022Article
- The Aggressive Diabetic Kidney Disease in Youth-Onset Type 2 Diabetes: Pathogenetic Mechanisms and Potential Therapies.Medicina (Kaunas, Lithuania) · 2021Review
- miR-30a-5p targets Becn1 to ameliorate high-glucose-induced glomerular podocyte injury in immortalized rat podocyte cell line.American journal of translational research · 2021Article
- Sleep Deprivation Interferes with JAK/STAT Signaling Pathway and Myogenesis in the Masseter Muscle of Rats.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2021Article
- Inhibition of interleukin-6 on matrix protein production by glomerular mesangial cells and the pathway involved.American journal of physiology. Renal physiology · 2020Article
- The Clinical Utility of Salivary Biomarkers in the Identification of Type 2 Diabetes Risk and Metabolic Syndrome.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-6 (IL-6) is a multifunctional cytokine that employs IL-6 classic and trans-signalling pathways, and these two signal channels execute different or even opposite effects in certain diseases. As a cardinal event of diabetic kidney disease (DKD), whether the podocyte abnormalities are associated with IL-6 signalling, especially classic or trans-signalling respectively, remains unclear. In this study, we identified that the circulatory IL-6, soluble IL-6R (sIL-6R) and soluble glycoprotein 130 (sgp130) levels are elevated in patients with DKD. The expressions of membrane-bound IL-6R (mIL-6R), sIL-6R and gp130 are enhanced in kidney cortex of diabetic mice accompanying with activated STAT3 by tyrosine 705 residue phosphorylation, while not serine 727. Above data infer both classic signalling and trans-signalling of IL-6 are activated during DKD. In cultured podocyte, high glucose (HG) up-regulates the expression of mIL-6R and gp130, as well as STAT3 tyrosine 705 phosphorylation, in a time-dependent manner. Entirely blocking IL-6 signalling by gp130 shRNA, gp130 or IL-6 neutralizing antibodies attenuates HG-induced podocyte injury. Interestingly, either inhibiting IL-6 classic signalling by mIL-6R shRNA or suppressing its trans-signalling using sgp130 protein dramatically alleviates HG-induced podocyte injury, suggesting both IL-6 classic signalling and trans-signalling play a detrimental role in HG-induced podocyte injury. Additionally, activation of IL-6 classic or trans-signalling aggravates podocyte damage in vitro. In summary, our observations demonstrate that the activation of either IL-6 classic or trans-signalling advances podocyte harming under hyperglycaemia. Thus, suppressing IL-6 classic and trans-signalling simultaneously may be more beneficial in podocyte protection and presents a novel therapeutic target for DKD.
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