ReviewNephron2023
Reprogramming Metabolism to Enhance Kidney Tolerance during Sepsis: The Role of Fatty Acid Oxidation, Aerobic Glycolysis, and Epithelial De-Differentiation.
Review in Nephron, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
18 citing papers in PubMed, 23 citations in OpenAlex.
- Twist Family BHLH Transcription Factor 1 orchestrates hypoxia-lactate crosstalk to bridge glycolytic flux and tubular maladaptation in fibrotic kidneys.Molecular biomedicine · 2026Article
- Research on Sepsis and Metabolic Reprogramming from 1998 to 2025: A Bibliometric and Visualized Analysis.Shock (Augusta, Ga.) · 2026Article
- Renal glucose metabolic enzyme expression during AKI-to-CKD transition.International urology and nephrology · 2026Article
- Hyperlactatemia in sepsis and shock: a renal metabolic perspective.Critical care (London, England) · 2026Review
- Immunometabolic Reprogramming in Experimental Sepsis: A Driver of Multiple Organ Dysfunction Syndrome.Journal of inflammation research · 2026Review
- Urinary cell cycle arrest biomarkers TIMP-2 and IGFBP7 for the assessment of acute kidney injury in dogs with pyometra.Frontiers in veterinary science · 2026Article
- Lipopolysaccharide-induced histone lactylation mediates m6A RNA modification causing mitochondrial dysfunction and pulmonary fibroblasts activation to exacerbate sepsis-associated pulmonary fibrosis.Respiratory research · 2025Article
- Human primary proximal tubular epithelial cells and sepsis: a scoping review.Clinical and experimental nephrology · 2025Article
- The role of natural products targeting macrophage polarization in sepsis-induced lung injury.Chinese medicine · 2025Review
- Exploring the role and therapeutic potential of lipid metabolism in acute kidney injury.Renal failure · 2024Review
- TREM2 aggravates sepsis by inhibiting fatty acid oxidation via the SHP1/BTK axis.The Journal of clinical investigation · 2024Article
- Renal tubular epithelial cells response to injury in acute kidney injury.EBioMedicine · 2024Review
- Effects of High-Mobility Group Box-1 on Mucosal Immunity and Epithelial Differentiation in Colitic Carcinoma.International journal of molecular sciences · 2024Article
- Sirtuins in kidney health and disease.Nature reviews. Nephrology · 2024Review
- Mitochondrial pyruvate carrier 2 mitigates acute kidney injury via sustaining mitochondrial metabolism.International journal of biological sciences · 2024Article
- The impact of glucose metabolism on inflammatory processes in sepsis-induced acute lung injury.Frontiers in immunology · 2024Review
- Article
- Proteomics reveals defective peroxisomal fatty acid oxidation during the progression of acute kidney injury and repair.Heliyon · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
backgroundThe recognition that sepsis induces acute kidney injury (AKI) in the absence of overt necrosis or apoptosis and even in the presence of increased renal blood flow has led to the consideration that kidney tubular epithelial cells (TECs) may deploy defense mechanisms to survive the insult. SUMMARY: This concept dovetails well with the notion that the defense against infection not only depends on the capacity of the immune system to limit the microbial burden or resistance capacity but also on the capacity of the host to limit tissue injury, collectively known as tolerance. To sustain the high energy requirement that ion transport mandates, kidney TECs use fatty acid oxidation (FAO) as one of the preferred sources of energy. Inflammatory processes like endotoxemia and sepsis decrease mitochondrial FAO and hinder mitochondrial respiration. Impaired FAO is associated with TEC de-differentiation, loss of kidney function, and TEC injury through lipotoxicity and oxidative stress in the acute setting, and with maladaptive repair and fibrosis after AKI in the latter stages. AMP-activated protein kinase (AMPK) is a master regulator of energy and promoter of FAO that can be activated pharmacologically to protect against AKI and death during experimental sepsis, operating through a tolerance mechanism. KEY MESSAGES: Organ dysfunction during sepsis is the expression of tissue injury and adaptive defense mechanisms operating through resistance or tolerance that prioritize cell survival over organ function. Metabolic reprogramming away from FAO/oxidative phosphorylation seems to be a common pathological denominator throughout the AKI continuum that may be targeted through the activation of AMPK.
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What Socratic holds
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 Socratic graph.