ArticleKidney international2024
Pax protein depletion in proximal tubules triggers conserved mechanisms of resistance to acute ischemic kidney injury preventing transition to chronic kidney disease.
Article in Kidney international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 14 citations in OpenAlex.
- Integrated bioinformatics and clinical validation of oxidative stress-associated genes in atrial fibrillation and chronic kidney disease.Experimental and therapeutic medicine · 2026Article
- Single-cell transcriptomic comparison of tubular segment maturation in advanced humaniScience · 2026Article
- Deletion of exocyst component 5 suppresses repair of injured kidney by limiting cell proliferation.Cell death discovery · 2026Article
- Matricellular protein SMOC2 safeguards tubular integrity in acute kidney injury via integrin β3-dependent inhibition of CCND1-CDK4/6 axis.Molecular biomedicine · 2026Article
- PAX gene expression in autosomal dominant polycystic kidney disease contributes to cyst expansion and regulates a gene network associated with cyst growth.Human molecular genetics · 2026Article
- Toward Combinatorial Strategies to Improve Proximal Tubule Recovery Following Acute Kidney Injury.Seminars in nephrology · 2026Review
- Chromatin remodeling and epigenetic regulation in chronic kidney disease.Frontiers in genetics · 2026Review
- Decreased parietal epithelial cell density is linked to podocyte depletion and predictors of kidney disease progression in human kidneys.American journal of physiology. Renal physiology · 2025Article
- SFPQ-TFE3 reciprocally regulates mTORC1 and induces lineage plasticity in a mouse model of renal tumorigenesis.Nature communications · 2025Article
- Pax inhibition: stressing proximal tubule for successful repair.American journal of physiology. Renal physiology · 2025Article
- Pax proteins mediate segment-specific functions in proximal tubule survival and response to ischemic injury.American journal of physiology. Renal physiology · 2025Article
- Multiomics profiling of mouse polycystic kidney disease progression at a single-cell resolution.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Sustained alterations in proximal tubule gene expression in primary culture associate with HNF4A loss.Scientific reports · 2024Article
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12 authors at 1 institution in 1 country.
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Abstract
Acute kidney injury (AKI) is a common condition that lacks effective treatments. In part, this shortcoming is due to an incomplete understanding of the genetic mechanisms that control pathogenesis and recovery. Identifying the molecular and genetic regulators unique to nephron segments that dictate vulnerability to injury and regenerative potential could lead to new therapeutic targets to treat ischemic kidney injury. Pax2 and Pax8 are homologous transcription factors with overlapping functions that are critical for kidney development and are re-activated in AKI. Here, we examined the role of Pax2 and Pax8 in recovery from ischemic AKI and found them upregulated after severe AKI and correlated with chronic injury. Surprisingly, proximal-tubule-selective deletion of Pax2 and Pax8 resulted in a less severe chronic injury phenotype. This effect was mediated by protection against the acute insult, similar to pre-conditioning. Prior to injury, Pax2 and Pax8 mutant mice develop a unique subpopulation of proximal tubule cells in the S3 segment that displayed features usually seen only in acute or chronic injury. The expression signature of these cells was strongly enriched with genes associated with other mechanisms of protection against ischemic AKI including caloric restriction, hypoxic pre-conditioning, and female sex. Thus, our results identified a novel role for Pax2 and Pax8 in mature proximal tubules that regulates critical genes and pathways involved in both the injury response and protection from ischemic AKI.
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