ArticleMolecular therapy : the journal of the American Society of Gene Therapy2022
Neat1 promotes acute kidney injury to chronic kidney disease by facilitating tubular epithelial cells apoptosis via sequestering miR-129-5p.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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35 citing papers in PubMed, 44 citations in OpenAlex.
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- Mechanisms of Obesity-Related Kidney Disease: From Adipose Depot Biology to the Chymase-Aldosterone and Ghrelin-Leptin Axes.Biomolecules · 2026Review
- Expression Landscape and Circadian Regulation of lncRNAs in the Kidney.Acta physiologica (Oxford, England) · 2026Article
- NAT10-mediated acCellular & molecular biology letters · 2026Article
- Long Non-Coding RNAs and Micro RNAs in Chronic Kidney Disease: Recent Advances and Future Directions-A 5-Year Systematic Review.Life (Basel, Switzerland) · 2026Review
- Small molecules targeting regulated cell death for chronic kidney disease therapy.Journal of pharmaceutical analysis · 2026Review
- From Single-Cell Clusters to Causality: ITCH Engagement for CKD Uncovered by Integrative Analysis of MR and MAGMA.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- FENDRR-mediated regulation of osteoclast differentiation through the miRNA-129-5p/P2X7R axis.Journal of orthopaedic surgery and research · 2026Article
- Astragaloside IV: A multipotent phytochemical for treating fibrotic diseases (Review).International journal of molecular medicine · 2026Review
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- From resistance to sensitivity: the impact of FADD and lncRNA PPFIA1-AS1 on cisplatin treatment in LUSC.Cancer gene therapy · 2026Article
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- Insights into organelle forming RNAs: Diversity, functions and future perspectives.Animal models and experimental medicine · 2025Review
- The NEAT1/miR-124-3p/CCL2 axis in chronic kidney disease progression: integrated bioinformatics analysis and experimental validation.Epigenomics · 2025Article
- Puerarin raises exosomal miR- 342 - 3p by inhibiting lncRNA NEAT1 in umbilical cord mesenchymal stem cells to alleviate renal tubular epithelial cell pyroptosis in chronic renal failure.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Role of the TGF‑β/Smad signaling pathway in the transition from acute kidney injury to chronic kidney disease (Review).International journal of molecular medicine · 2025Review
- PARylation promotes acute kidney injuryActa pharmaceutica Sinica. B · 2025Article
- Targeting PARylated RACK1/HIF-1Acta pharmaceutica Sinica. B · 2025Article
- The role of lncRNAs in AKI and CKD: Molecular mechanisms, biomarkers, and potential therapeutic targets.Genes & diseases · 2025Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is increasingly identified as a crucial risk factor for progression to CKD. However, the factors governing AKI to CKD progression remain largely unknown. By high-throughput RNA sequencing, we found that Neat1_2, a transcript variant of Neat1, was upregulated in 40-min ischemia/reperfusion injury (IRI), which resulted in the development of renal fibrotic lesions. The upregulation of Neat1_2 in hypoxia-treated TECs was attributed to p53 transcriptional regulation. Gain- and loss-of-function studies, both in vitro and in vivo, demonstrated that Neat1_2 promoted apoptosis of injured TECs induced by IRI and caused tubulointerstitial inflammation and fibrosis. Mechanistically, Neat1_2 shares miRNA response elements with FADD, CASP-8, and CASP-3. Neat1_2 competitively binds to miR-129-5p and prevents miR-129-5p from decreasing the levels of FADD, CASP-8, and CASP-3, and ultimately facilitates TEC apoptosis. Increased expression of Neat1_2 associated with kidney injury and TEC apoptosis was recapitulated in human AKI, highlighting its clinical relevance. These findings suggest that preventing TEC apoptosis by hindering Neat1_2 expression may be a potential therapeutic strategy for AKI to CKD progression.
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