ArticleJournal of cellular and molecular medicine2018
TAK1 mediates excessive autophagy via p38 and ERK in cisplatin-induced acute kidney injury.
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. An erratum has been issued. Cited by 32 papers.
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32 citing papers in PubMed, 54 citations in OpenAlex.
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- Long noncoding RNA MALAT1 can regulate proliferation and apoptosis of LPS-treated HK-2 cells via targeting miR-23a-3p through regulating ERK signaling.Archives of medical science : AMS · 2025Article
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- PARVB deficiency alleviates cisplatin-induced tubular injury by inhibiting TAK1 signaling.Cellular and molecular life sciences : CMLS · 2024Article
- Bibliometric and visualized analysis on global trends and hotspots of TAK1 in regulated cell death: 1999 to 2024.Frontiers in immunology · 2024Article
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- LncRNAs in non-small cell lung cancer: novel diagnostic and prognostic biomarkers.Frontiers in molecular biosciences · 2023Review
- Chemotherapy-induced nephrotoxicity was improved by crocin in mouse model.European journal of histochemistry : EJH · 2022Article
- Pro-Inflammatory Signalling PRRopels Cisplatin-Induced Toxicity.International journal of molecular sciences · 2022Review
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- Identification of Smad3-related transcriptomes in type-2 diabetic nephropathy by whole transcriptome RNA sequencing.Journal of cellular and molecular medicine · 2021Article
- Sulforaphane Inhibits Osteoclastogenesis via Suppression of the Autophagic Pathway.Molecules (Basel, Switzerland) · 2021Article
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- Acute liver failure is regulated by MYC- and microbiome-dependent programs.Nature medicine · 2020Article
- Effects of tacrolimus on autophagy protein LC3 in puromycin-damaged mouse podocytes.The Journal of international medical research · 2020Article
- Heat-KilledJournal of microbiology and biotechnology · 2020Article
- SQSTM1/p62 Controls mtDNA Expression and Participates in Mitochondrial Energetic Adaption via MRPL12.iScience · 2020Article
- Microglial-specific depletion of TAK1 is neuroprotective in the acute phase after ischemic stroke.Journal of molecular medicine (Berlin, Germany) · 2020Article
- Protein phosphatase 6 is a key factor regulating spermatogenesis.Cell death and differentiation · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ability of cisplatin (cis-diamminedichloroplatinum II) toxicity to induce acute kidney injury (AKI) has attracted people's attention and concern for a long time, but its molecular mechanisms are still widely unknown. We found that the expression of transforming growth factor-β (TGF-β)-activated kinase 1 (TAK1) could be increased in kidneys of mice administrated with cisplatin. Autophagy is an evolutionarily conserved catabolic pathway and is involved in various acute and chronic injuries. Moreover, p38 MAPK (mitogen-activated protein kinase) and ERK regulate autophagy in response to various stimuli. Therefore, our hypothesis is that cisplatin activates TAK1, which phosphorylates p38 and ERK, leading to excessive autophagy of tubular epithelial cells and thus exacerbating kidney damage. Here, BALB/c mice were intraperitoneally injected with a TAK1 inhibitor and were then administrated with sham or cisplatin at 20 mg/kg by intraperitoneal injection. Compared with mice in the vehicle cisplatin group, mice intraperitoneally injected with a TAK1 inhibitor were found to have lower serum creatinine and less tubular damage following cisplatin-induced AKI. Furthermore, inhibition of TAK1 reduced p38 and Erk phosphorylation, decreased expression of LC3II and reversed the down-regulation of P62 expression induced by cisplatin. The hypothesis was verified with tubular epithelial cells administrated with cisplatin in vitro. Finally, p38 inhibitor or ERK inhibitor abated autophagy activation and cell viability reduction in tubular epithelial cells treated with cisplatin plus TAK1 overexpression vector. Taken together, our results show that cisplatin activates TAK1, which phosphorylates p38 and ERK, leading to excessive autophagy of tubular epithelial cells that exacerbates kidney damage.
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