ReviewJournal of clinical medicine2021
Metabolic Reprogramming and Host Tolerance: A Novel Concept to Understand Sepsis-Associated AKI.
Review in Journal of clinical medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 29 citations in OpenAlex.
- Anion gap trajectory patterns and prognosis in sepsis patients: A multicenter retrospective study.Medicine · 2026Article
- Cardiovascular and Autonomic Phenotypes Reveal Distinct Mechanisms of Sepsis Decompensation via Deep Learning.Research square · 2026Article
- Does hypoxemia aggravate sepsis-associated acute kidney injury? Integrated clinical and experimental evidence.Intensive care medicine experimental · 2025Article
- Research Progress on Signalling Pathways Related to Sepsis-Associated Acute Kidney Injury in Children.Current issues in molecular biology · 2025Review
- Beyond inflammation: the role of metabolic dysregulation in sepsis diagnosis and treatment.Intensive care medicine · 2025Article
- The Role of Mitochondrial Dysfunction in Sepsis-Associated Acute Kidney Injury: A Narrative Review.Drug design, development and therapy · 2025Review
- Review of research progress in sepsis-associated acute kidney injury.Frontiers in molecular biosciences · 2025Review
- Sepsis-Associated Acute Kidney Injury: What's New Regarding Its Diagnostics and Therapeutics?Diagnostics (Basel, Switzerland) · 2024Review
- Sepsis-Associated Acute Kidney Injury: Where Are We Now?Medicina (Kaunas, Lithuania) · 2024Review
- Mitochondrial pyruvate carrier 2 mitigates acute kidney injury via sustaining mitochondrial metabolism.International journal of biological sciences · 2024Article
- Advances in metabolic reprogramming of renal tubular epithelial cells in sepsis-associated acute kidney injury.Frontiers in physiology · 2024Review
- Evaluation of urinary neutrophil gelatinase associated lipocalin in the early diagnosis of acute kidney injury with sepsis.American journal of translational research · 2024Article
- The Values of PDK1 and LDH Levels in Patients with Sepsis and Septic Shock: A Prospective Observational Study.Journal of inflammation research · 2024Article
- The role of inflammatory response and metabolic reprogramming in sepsis-associated acute kidney injury: mechanistic insights and therapeutic potential.Frontiers in immunology · 2024Review
- Role of heparanase in sepsis‑related acute kidney injury (Review).Experimental and therapeutic medicine · 2023Review
- Lack of change in the respiratory quotient during oxygen supply dependence in endotoxemic shock: a subanalysis of an experimental controlled study.Critical care science · 2023Article
- Vitamin D-Frontiers in physiology · 2023Article
- Review
- Review
- Tubular Mitochondrial Dysfunction, Oxidative Stress, and Progression of Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Acute kidney injury (AKI) is a frequent complication of sepsis that increases mortality and the risk of progression to chronic kidney disease. However, the mechanisms leading to sepsis-associated AKI are still poorly understood. The recognition that sepsis induces organ dysfunction in the absence of overt necrosis or apoptosis has led to the consideration that tubular epithelial cells (TEC) may deploy defense mechanisms to survive the insult. This concept dovetails well with the notion that the defense against infection does not only depend on the capacity of the immune system to limit the microbial load (known as resistance), but also on the capacity of cells and tissues to limit tissue injury (known as tolerance). In this review, we discuss the importance of TEC metabolic reprogramming as a defense strategy during sepsis, and how this cellular response is likely to operate through a tolerance mechanism. We discuss the fundamental role of specific regulatory nodes and of mitochondria in orchestrating this response, and how this opens avenues for the exploration of targeted therapeutic strategies to prevent or treat sepsis-associated AKI.
Indexed as
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What OpenQuestion 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 OpenQuestion graph.