ArticleJCI insight2023
Mitochondrial and NAD+ metabolism predict recovery from acute kidney injury in a diverse mouse population.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Effects of NAD⁺ repletion with Nicotinamide riboside on obesity-induced chronic kidney disease and renal cell lipotoxicity.Scientific reports · 2026Article
- Antagonism of Kinin Receptors B1 and B2 Attenuates Folic Acid-Induced Tubulointerstitial Fibrosis in Mice.Basic & clinical pharmacology & toxicology · 2026Article
- Pulsed ultrasound targeted to the spleen mitigates against kidney injury and promotes kidney repair.American journal of physiology. Renal physiology · 2025Article
- Mitochondrial SLC3A1 regulates sexual dimorphism in cystinuria.Genes & diseases · 2025Article
- New evidence of the impact of mitochondria on kidney health and disease.Nature reviews. Nephrology · 2024Article
- Tubular deficiency of ABCA1 augments cholesterol- and NaAmerican journal of physiology. Renal physiology · 2024Article
- The Physiological and Pathological Role of Acyl-CoA Oxidation.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney failure and chronic kidney disease are global health issues steadily rising in incidence and prevalence. Animal models on a single genetic background have so far failed to recapitulate the clinical presentation of human nephropathies. Here, we used a simple model of folic acid-induced kidney injury in 7 highly diverse mouse strains. We measured plasma and urine parameters, as well as renal histopathology and mRNA expression data, at 1, 2, and 6 weeks after injury, covering the early recovery and long-term remission. We observed an extensive strain-specific response ranging from complete resistance of the CAST/EiJ to high sensitivity of the C57BL/6J, DBA/2J, and PWK/PhJ strains. In susceptible strains, the severe early kidney injury was accompanied by the induction of mitochondrial stress response (MSR) genes and the attenuation of NAD+ synthesis pathways. This is associated with delayed healing and a prolonged inflammatory and adaptive immune response 6 weeks after insult, heralding a transition to chronic kidney disease. Through a thorough comparison of the transcriptomic response in mouse and human disease, we show that critical metabolic gene alterations were shared across species, and we highlight the PWK/PhJ strain as an emergent model of transition from acute kidney injury to chronic disease.
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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.