ReviewAmerican journal of physiology. Renal physiology2022
Mitochondria as mediators of systemic inflammation and organ cross talk in acute kidney injury.
Review in American journal of physiology. Renal physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05960227 (Effect of Intravenous Iron Repletion on Renal Function in Patients With Iron Deficiency and Acute Kidney Injury, Clinical Trial), which is not on this 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.
Effect of Intravenous Iron Repletion on Renal Function in Patients With Iron Deficiency and Acute Kidney Injury, Clinical Trial
Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Effect of Intravenous Iron Dextran on Kidney Outcomes in Acute Kidney Injury with Iron Deficiency: A Randomized Trial.Kidney360 · 2026Trial
- Allopurinol mitigates distant organ damage following bilateral renal ischemia-reperfusion injury in male rats.BMC nephrology · 2026Article
- Development and validation of a bedside prognostic model for in-hospital mortality in acute diquat poisoning.BMC emergency medicine · 2026Article
- Mitochondrial Dysfunction in Acute Kidney Injury: Intersections Between Chemotherapy and Novel Cancer Immunotherapies.Biomolecules · 2026Review
- Midkine-Mediated Microglia Activation after Renal Injury Promotes Cognitive Impairment Following Ischemic Renal Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Kidney-organ interactions: recent advances and clinical implications.Current opinion in critical care · 2025Review
- Organ Crosstalk During Injury: Mechanisms of Lung-Kidney Interaction in Critical Illness.Comprehensive Physiology · 2025Review
- Mechanisms of lung crosstalk with end organs: scientific session V-ReSPIRE 2025.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- Article
- Human pulmonary microvascular endothelial cells respond to DAMPs from injured renal tubular cells.Pulmonary circulation · 2024Article
- Association between glycemic variability and short-term mortality in patients with acute kidney injury: a retrospective cohort study of the MIMIC-IV database.Scientific reports · 2024Article
- Bidirectional pressure: a mini review of ventilator-lung-kidney interactions.Frontiers in physiology · 2024Review
- Prognostic Value of the Baseline and Early Changes in Monocyte-to-Lymphocyte Ratio for Short-Term Mortality among Critically Ill Patients with Acute Kidney Injury.Journal of clinical medicine · 2023Article
- Autophagy and mitophagy: physiological implications in kidney inflammation and diseases.American journal of physiology. Renal physiology · 2023Review
- SerpinA3K Deficiency Reduces Oxidative Stress in Acute Kidney Injury.International journal of molecular sciences · 2023Article
- Renal Denervation Helps Preserve the Ejection Fraction by Preserving Endocardial-Endothelial Function during Heart Failure.International journal of molecular sciences · 2023Article
- Article
- Roles of Mitochondrial DNA Damage in Kidney Diseases: A New Biomarker.International journal of molecular sciences · 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
Acute kidney injury (AKI) is a systemic inflammatory disease that contributes to remote organ failures. Multiple organ failure is the leading cause of death due to AKI, and lack of understanding of the mechanisms involved has precluded the development of novel therapies. Mitochondrial injury in AKI leads to mitochondrial fragmentation and release of damage-associated molecular patterns, which are known to active innate immune pathways and systemic inflammation. This review presents current evidence suggesting that extracellular mitochondrial damage-associated molecular patterns are mediators of remote organ failures during AKI that have the potential to be modifiable.
Indexed as
Identifiers
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.