ReviewFrontiers in physiology2024
Advances in metabolic reprogramming of renal tubular epithelial cells in sepsis-associated acute kidney injury.
Review in Frontiers in physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Mitochondrial dysfunction in sepsis: nutritional strategies for restoring bioenergetic homeostasis.Frontiers in cellular and infection microbiology · 2026Pooled it
- Gut microbiota metabolic reprogramming drives the development of metabolic diseases in the host.Gut microbes · 2026Review
- Lactate in acute kidney injury: pathobiology, risk stratification, and clinical interpretation.Renal failure · 2026Review
- Mitochondrial lipid remodeling in sepsis-associated acute kidney injury: a cardiolipin-centered convergence framework.Archives of toxicology · 2026Review
- From AKI to CKD mechanisms of maladaptive repair and disease progression.International urology and nephrology · 2026Review
- Renal Tubular Epithelial Cells as Central Hubs of Kidney Disease.Diagnostics (Basel, Switzerland) · 2026Review
- Cell death in sepsis: unveiling new perspectives on organ dysfunction.Frontiers in cell and developmental biology · 2026Review
- Pathological triad of perioperative acute kidney injury: renal microcirculatory hypoxia, mitochondrial damage, and immuno-metabolic reprogramming.Frontiers in immunology · 2026Review
- Beyond angiogenesis: integrating ferroptosis and metabolic rewiring for next-generation RCC therapy.Frontiers in oncology · 2026Review
- Mitochondrial dysfunction in sepsis-induced immunoparalysis: from immune-cell metabolic reprogramming to clinical biomarkers.Frontiers in immunology · 2026Review
- Association of Serum Lactate Dehydrogenase With Sepsis-Associated Acute Kidney Injury: A Large-Scale Analysis Based on the MIMIC-IV Database.Emergency medicine international · 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
- Association between the atherogenic index of plasma and acute kidney injury in sepsis patients.PloS one · 2026Article
- METTL3-driven mFrontiers in immunology · 2026Article
- Targeting renal tubular epithelial cellsActa pharmaceutica Sinica. B · 2025Article
- Mesenchymal stem cells in sepsis-induced organ dysfunction: mechanisms and therapeutic potential.Stem cell research & therapy · 2025Review
- Fenofibrate alleviates sepsis-associated acute kidney injury by enhancing renal fatty acid oxidation.BMC pharmacology & toxicology · 2025Article
- Exploring the molecular mechanisms of lactylation-related biological functions and immune regulation in sepsis-associated acute kidney injury.Clinical and experimental medicine · 2025Article
- The Role of Mitochondrial Dysfunction in Sepsis-Associated Acute Kidney Injury: A Narrative Review.Drug design, development and therapy · 2025Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-associated acute kidney injury presents as a critical condition characterized by prolonged hospital stays, elevated mortality rates, and an increased likelihood of transition to chronic kidney disease. Sepsis-associated acute kidney injury suppresses fatty acid oxidation and oxidative phosphorylation in the mitochondria of renal tubular epithelial cells, thus favoring a metabolic shift towards glycolysis for energy production. This shift acts as a protective mechanism for the kidneys. However, an extended reliance on glycolysis may contribute to tubular atrophy, fibrosis, and subsequent chronic kidney disease progression. Metabolic reprogramming interventions have emerged as prospective strategies to counteract sepsis-associated acute kidney injury by restoring normal metabolic function, offering potential therapeutic and preventive modalities. This review delves into the metabolic alterations of tubular epithelial cells associated with sepsis-associated acute kidney injury, stressing the importance of metabolic reprogramming for the immune response and the urgency of metabolic normalization. We present various intervention targets that could facilitate the recovery of oxidative phosphorylation-centric metabolism. These novel insights and strategies aim to transform the clinical prevention and treatment landscape of sepsis-associated acute kidney injury, with a focus on metabolic mechanisms. This investigation could provide valuable insights for clinicians aiming to enhance patient outcomes in the context of sepsis-associated acute kidney injury.
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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.