ArticleScience signaling2019
Metabolic rewiring of the hypertensive kidney.
Article in Science signaling, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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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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.
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Who cites it
42 citing papers in PubMed, 70 citations in OpenAlex.
- Article
- Podocyte Metabolic Reprogramming and Targeted Therapy.Journal of the American Society of Nephrology : JASN · 2026Review
- MCD enzyme deficiency drives early mortality and multiorgan metabolic disruption in Dahl salt-sensitive rats.iScience · 2026Article
- Gut-to-brain signaling restricts dietary protein intake during recovery from catabolic states.Cell · 2025Article
- Multi-omics revealed GOT1/ALDH3A1 pathway attenuated head and neck squamous cell carcinoma and increased cisplatin sensitivity through ROS induced by mitochondrial dysfunction.Redox report : communications in free radical research · 2025Article
- Temporal glomerular gene expression dynamics during disease progression in a mouse model of hypertension-accelerated diabetic kidney disease.Animal models and experimental medicine · 2025Article
- The role of carnitine palmitoyl transferase 2 in the progression of salt-sensitive hypertension.American journal of physiology. Cell physiology · 2025Article
- Human plasma metabolomics reveals metabolic targets for intervention in salt-sensitive hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2025Article
- Longitudinal Multi-Organ Transcriptomic Atlas of Salt-Induced Hypertension.bioRxiv : the preprint server for biology · 2025Article
- Exploring population and sex-specific disease trajectories for multimorbidities among individuals with overweight or obesity: A retrospective cohort study in UK biobank.Diabetes, obesity & metabolism · 2025Article
- Beyond Blood Pressure: Emerging Pathways and Precision Approaches in Hypertension-Induced Kidney Damage.International journal of molecular sciences · 2025Review
- Review
- A brief harvesting-freezing delay significantly alters the kidney metabolome and leads to false positive and negative results.American journal of physiology. Renal physiology · 2024Article
- Deletion ofiScience · 2024Article
- Perspectives on the involvement of the gut microbiota in salt-sensitive hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Review
- Observational
- Genetic imputation of kidney transcriptome, proteome and multi-omics illuminates new blood pressure and hypertension targets.Nature communications · 2024Article
- Transcriptomic changes in glomeruli in response to a high salt challenge in the Dahl SS rat.Physiological genomics · 2024Article
- Renal Epithelial Mitochondria: Implications for Hypertensive Kidney Disease.Comprehensive Physiology · 2023Article
- How is Big Data reshaping preclinical aging research?Lab animal · 2023Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Hypertension is a persistent epidemic across the developed world that is closely associated with kidney disease. Here, we applied a metabolomic, phosphoproteomic, and proteomic strategy to analyze the effect of hypertensive insults on kidneys. Our data revealed the metabolic aspects of hypertension-induced glomerular sclerosis, including lipid breakdown at early disease stages and activation of anaplerotic pathways to regenerate energy equivalents to counter stress. For example, branched-chain amino acids and proline, required for collagen synthesis, were depleted in glomeruli at early time points. Furthermore, indicators of metabolic stress were reflected by low amounts of ATP and NADH and an increased abundance of oxidized lipids derived from lipid breakdown. These processes were specific to kidney glomeruli where metabolic signaling occurred through mTOR and AMPK signaling. Quantitative phosphoproteomics combined with computational modeling suggested that these processes controlled key molecules in glomeruli and specifically podocytes, including cytoskeletal components and GTP-binding proteins, which would be expected to compete for decreasing amounts of GTP at early time points. As a result, glomeruli showed increased expression of metabolic enzymes of central carbon metabolism, amino acid degradation, and lipid oxidation, findings observed in previously published studies from other disease models and patients with glomerular damage. Overall, multilayered omics provides an overview of hypertensive kidney damage and suggests that metabolic or dietary interventions could prevent and treat glomerular disease and hypertension-induced nephropathy.
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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.