ReviewFrontiers in cell and developmental biology2023
Energy metabolic reprogramming regulates programmed cell death of renal tubular epithelial cells and might serve as a new therapeutic target for acute kidney injury.
Review in Frontiers in cell and developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Metabolomics biomarkers and related pathways in acute renal injury: a bibliometric investigation, meta-analysis, and systematic review.Frontiers in medicine · 2025Pooled it
- Advancements in early biomarkers of acute kidney injury: from traditional indicators to a paradigm shift in lactate metabolism.Annals of medicine · 2026Review
- Programmed cell death in kidney disease: integrated crosstalk among ferroptosis, pyroptosis, apoptosis, and cuproptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Integrating Bulk and Single-Cell RNA Sequencing Identifies and Validates Lactylation-Related Signatures in Acute Kidney Injury.Biomedicines · 2026Article
- SLC38A6 expression in renal tubular cells accelerates cisplatin-induced acute kidney injury by promoting cell apoptosis.The FEBS journal · 2026Article
- Mitochondrial lipid remodeling in sepsis-associated acute kidney injury: a cardiolipin-centered convergence framework.Archives of toxicology · 2026Review
- RNA biomarker signatures for prediction of acute kidney injury in acute coronary syndrome patients undergoing PCI.BMC nephrology · 2026Observational
- Integrating metabolomics and machine learning with in silico analysis to identify early biomarkers and molecular interactions in sepsis-associated acute kidney injury.Scientific reports · 2026Article
- Review
- Chronic NHScientific reports · 2026Article
- Temporal Proteomic and Phosphoproteomic Profiling Deciphers Molecular Dynamics of Acute-to-Chronic Kidney Disease After Ischemia-Reperfusion Injury, With Dock2 Emerging as a Key Regulator.Molecular & cellular proteomics : MCP · 2026Article
- Optimization of M1 macrophage targeting using a glucosylated albumin nanoplatform for ROS scavenging and mitochondrial rescue in acute kidney injury.Journal of nanobiotechnology · 2026Article
- Current Status and Future Prospects of Research on Sepsis-Related Acute Kidney Injury.International journal of molecular sciences · 2026Review
- A pan-cancer atlas of metabolic regulatory circuitries integrating multi-omic, immune, and clinical dimensions.Frontiers in molecular biosciences · 2026Article
- Apoptosis, Pyroptosis, and Necroptosis (PANoptosis) may be Present in Renal Ischemic Injury.Current medicinal chemistry · 2026Article
- Fucoxanthin Ameliorates Diabetic Kidney Disease via Modulating the Gut Microbiota and Tryptophan-Kynurenine Metabolic Pathway.Journal of immunology research · 2026Article
- Cellular senescence of renal tubular epithelial cells in diabetic kidney disease: emerging mechanisms and targeted interventions.Frontiers in cell and developmental biology · 2026Review
- S100A12 drives inflammatory and metabolic reprogramming in sepsis-associated acute kidney injury.Frontiers in molecular biosciences · 2026Review
- High-fructose diet induces depressive-like behaviors and short-term memory deficits through hippocampal neurogenesis impairment via neural stem cell dysfunction.Nutrition & metabolism · 2025Article
- Association between time-weighted average glucose concentration or glucose variability and acute kidney injury among coronary artery disease patients with prediabetes.Renal failure · 2025Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) induces significant energy metabolic reprogramming in renal tubular epithelial cells (TECs), thereby altering lipid, glucose, and amino acid metabolism. The changes in lipid metabolism encompass not only the downregulation of fatty acid oxidation (FAO) but also changes in cell membrane lipids and triglycerides metabolism. Regarding glucose metabolism, AKI leads to increased glycolysis, activation of the pentose phosphate pathway (PPP), inhibition of gluconeogenesis, and upregulation of the polyol pathway. Research indicates that inhibiting glycolysis, promoting the PPP, and blocking the polyol pathway exhibit a protective effect on AKI-affected kidneys. Additionally, changes in amino acid metabolism, including branched-chain amino acids, glutamine, arginine, and tryptophan, play an important role in AKI progression. These metabolic changes are closely related to the programmed cell death of renal TECs, involving autophagy, apoptosis, necroptosis, pyroptosis, and ferroptosis. Notably, abnormal intracellular lipid accumulation can impede autophagic clearance, further exacerbating lipid accumulation and compromising autophagic function, forming a vicious cycle. Recent studies have demonstrated the potential of ameliorating AKI-induced kidney damage through calorie and dietary restriction. Consequently, modifying the energy metabolism of renal TECs and dietary patterns may be an effective strategy for AKI treatment.
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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.