ArticleAmerican journal of physiology. Renal physiology2021
IFT88 deficiency in proximal tubular cells exaggerates cisplatin-induced injury by suppressing autophagy.
Article in American journal of physiology. Renal physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Selective autophagy in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Ift46 deficiency causes renal cyst via enhanced Limk2 through lack of autophagy flux.Cell communication and signaling : CCS · 2026Article
- Cholangiocytes' primary cilia regulate DNA damage response and repair.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Differentially expressed ncRNAs as key regulators in infection of human bronchial epithelial cells by the SARS-CoV-2 Delta variant.Molecular therapy. Nucleic acids · 2025Article
- Cilia-deficient renal tubule cells are primed for injury with mitochondrial defects and aberrant tryptophan metabolism.American journal of physiology. Renal physiology · 2024Article
- Deficiency of the Planar Cell Polarity Protein Intu Delays Kidney Repair and Suppresses Renal Fibrosis after Acute Kidney Injury.The American journal of pathology · 2023Article
- Pharmacological inhibitors of autophagy have opposite effects in acute and chronic cisplatin-induced kidney injury.American journal of physiology. Renal physiology · 2022Article
- Organelle Stress and Metabolic Derangement in Kidney Disease.International journal of molecular sciences · 2022Review
- Multiomic identification of factors associated with progression to cystic kidney disease in mice with nephron Ift88 disruption.American journal of physiology. Renal physiology · 2022Article
- Autophagy and the primary cilium in cell metabolism: What's upstream?Frontiers in cell and developmental biology · 2022Review
- Development of an autophagy activator from Class III PI3K complexes, Tat-BECN1 peptide: Mechanisms and applications.Frontiers in cell and developmental biology · 2022Review
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Authors and funding
3 authors at 2 institutions in 1 country.
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Abstract
Primary cilia are widely regarded as specialized sensors in differentiated cells that have been implicated in the regulation of cell proliferation, differentiation, and viability. We have previously shown that shortening of primary cilia sensitizes cultured kidney tubular cells to cisplatin-induced apoptosis. Intraflagellar transport 88 (IFT88) is an essential component for ciliogenesis and maintenance. Here, we have further examined the effect of proximal tubule-specific IFT88 ablation on cisplatin-induced acute kidney injury (AKI). In this study, more severe AKI occurred in IFT88 knockout mice than age- and sex-matched wild-type mice. Mechanistically, cisplatin stimulated autophagy in kidney tubular cells as an intrinsic protective mechanism. However, renal autophagy was severely impaired in IFT88 knockout mice. In cultured HK-2 cells, cisplatin induced more apoptosis when IFT88 was knocked down. Tat-beclin 1 peptide, a specific autophagy activator, could partially prevent IFT88-associated cell death during cisplatin treatment, although cilium length was not improved significantly. Reexpression of IFT88 partially restored autophagy in IFT88 knockdown cells and suppressed apoptosis during cisplatin treatment. Taken together, these results indicate that defective autophagy in IFT88-deficient kidney cells and tissues contributes to the exaggerated AKI following cisplatin exposure.
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