ArticleThe Journal of clinical investigation2024
Targeting de novo lipogenesis to mitigate kidney disease.
Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Senescent hepatic stellate cells drive inflammation and disease progression in MASH (Review).Experimental and therapeutic medicine · 2026Review
- Hypertriglyceridemia in chronic kidney disease: pathophysiological mechanisms, cardiovascular risk, and emerging therapeutics.Lipids in health and disease · 2026Review
- Ectopic lipid deposition in kidney diseases: mechanisms in specific cell types and therapeutic strategies.Frontiers in endocrinology · 2026Review
- Renal tubular epithelial IGFBP7 interacts with PKM2 to drive renal lipid accumulation and fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- ACSS2 protects against alcohol-induced hepatocyte ferroptosis through regulation of hepcidin expression.Nature communications · 2025Article
- The transcriptome of early compensatory kidney growth reveals cell and time specific responses.iScience · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Ten percent of the population worldwide suffers from chronic kidney disease (CKD), but the mechanisms driving CKD pathology are incompletely understood. While dysregulated lipid metabolism is one hallmark of CKD, the pathogenesis of cellular lipid accumulation remains unclear. In this issue of the JCI, Mukhi et al. Identify acyl-CoA synthetase short-chain family 2 (ACSS2) as a disease risk gene and demonstrate a role for ACSS2 in de novo lipogenesis (DNL). Notably, genetic or pharmacological inhibition of DNL protected against kidney disease progression in mice. These findings warrant evaluation of DNL inhibition with respect to efficacy and safety in people with CKD.
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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.