ArticleNature communications2023
Polynucleotide phosphorylase protects against renal tubular injury via blocking mt-dsRNA-PKR-eIF2α axis.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 29 citations in OpenAlex.
- Mitochondrial dysfunction-ferroptosis crosstalk drives renal fibrosis in chronic kidney disease.Renal failure · 2026Review
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- Interferon-λ drives renal fibrosis by coordinating epithelial-fibroblast crosstalk.The Journal of experimental medicine · 2026Article
- FOSL1 upregulation contributes to ischemia/reperfusion-induced acute kidney injury by regulating GPX4-dependent ferroptosis.Biology direct · 2026Article
- Mitochondrial ncRNAs: From Pathological Regulation to Targeted Therapy in Cardiovascular Diseases.Journal of cardiovascular translational research · 2026Review
- Mitochondrial dysfunction activates ADAMTS-5 expression via mt-dsRNA-PKR-Spi-1 axis in osteoarthritic chondrocytes.iScience · 2026Article
- Interferon-alpha selectively signals mitochondrial pore opening to allow mitochondrial RNA release in systemic lupus erythematosus: pathophysiological implications.Cell communication and signaling : CCS · 2026Article
- Renal tubular VMP1 protects against acute kidney injury via modulating autophagy and autophagy-independent pathway.Autophagy · 2025Article
- Taurine can restrict MtdsRNA mediated pyroptosis by enhancing mitophagy in nucleus pulposus cells.Cell communication and signaling : CCS · 2025Article
- Loss of glomerular aldolase B in diabetic nephropathy promotes renal fibrosis via activating Akt/GSK/β-catenin axis.Journal of advanced research · 2025Article
- Human polynucleotide phosphorylase in mitochondrial RNA metabolism.Bioscience reports · 2025Review
- Neutrophil extracellular trap-derived double-stranded RNA aggravates PANoptosis in renal ischemia reperfusion injury.Cell communication and signaling : CCS · 2025Article
- Mechanisms and effects of activation of innate immunity by mitochondrial nucleic acids.International immunology · 2025Review
- Unleashing viral mimicry: A combinatorial strategy to enhance the efficacy of PARP7 inhibitors.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Mitochondrial RNA in Inflammation.International journal of biological sciences · 2025Review
- Mitochondrial double-stranded RNA homeostasis depends on cell-cycle progression.Life science alliance · 2024Article
- IBR1, a novel endogenous IFIH1-binding dsRNA, governs IFIH1 activation and M1 macrophage polarisation in ARDS.Clinical and translational medicine · 2024Article
- Release of mitochondrial dsRNA into the cytosol is a key driver of the inflammatory phenotype of senescent cells.Nature communications · 2024Article
- RNA 5-methylcytosine marks mitochondrial double-stranded RNAs for degradation and cytosolic release.Molecular cell · 2024Article
- PKR Mediates the Mitochondrial Unfolded Protein Response through Double-Stranded RNA Accumulation under Mitochondrial Stress.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal tubular atrophy is a hallmark of chronic kidney disease. The cause of tubular atrophy, however, remains elusive. Here we report that reduction of renal tubular cell polynucleotide phosphorylase (PNPT1) causes renal tubular translation arrest and atrophy. Analysis of tubular atrophic tissues from renal dysfunction patients and male mice with ischemia-reperfusion injuries (IRI) or unilateral ureteral obstruction (UUO) treatment shows that renal tubular PNPT1 is markedly downregulated under atrophic conditions. PNPT1 reduction leads to leakage of mitochondrial double-stranded RNA (mt-dsRNA) into the cytoplasm where it activates protein kinase R (PKR), followed by phosphorylation of eukaryotic initiation factor 2α (eIF2α) and protein translational termination. Increasing renal PNPT1 expression or inhibiting PKR activity largely rescues IRI- or UUO-induced mouse renal tubular injury. Moreover, tubular-specific PNPT1-knockout mice display Fanconi syndrome-like phenotypes with impaired reabsorption and significant renal tubular injury. Our results reveal that PNPT1 protects renal tubules by blocking the mt-dsRNA-PKR-eIF2α axis.
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Registered trials
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.