ArticleCell death discovery2025
NRF1 coordinates mitochondrial adaptations to dampen intracellular ROS and inflammatory responses during ischemia reperfusion.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Hyperbaric Oxygen Attenuates Cerebral Ischemia-Reperfusion Injury Through ROS-Dependent Remodeling of Microglial Mitochondrial Dynamics.International journal of molecular sciences · 2026Article
- Advances in electroacupuncture for perioperative neurocognitive disorders: mechanisms and clinical evidence.Chinese medicine · 2026Review
- Peptide nanoarchitectonics of biomimetic nanozyme synergistically inhibits smooth muscle cell proliferation and promotes endothelial repair to reduce poststenting complications.Journal of nanobiotechnology · 2026Article
- Cholesterol-driven mitochondrial rejuvenation by quercetin nanotherapeutics restores implant osseointegration in diabetes.Bioactive materials · 2026Article
- A multifunctional and ROS response CO-gas delivery platform for spinal cord regeneration.Materials today. Bio · 2026Article
- Nuclear Respiratory Factor-1 Ameliorates Heart Failure by Suppressing Cardiomyocyte Pyroptosis-Associated Signaling Via the Downregulation of Gasdermin D and Caspase-1.Cardiology research · 2026Article
- The role and therapeutic potential of succinate and succinylation in cardiovascular diseases.Clinical epigenetics · 2026Review
- Oxidative Stress in Diabetic Cardiomyopathy: Molecular Mechanisms and Emerging Therapeutic Targets.Biomolecules · 2026Review
- Smarca4 maintains mitochondrial homeostasis and energy metabolism during cardiac development.Cellular and molecular life sciences : CMLS · 2026Article
- HIF1A transcriptionally activates CDKN1A to drive ferroptosis in skeletal muscle ischaemia-reperfusion injury.Journal of orthopaedic translation · 2026Article
- The Influence of Sex and Hormones on Organelle Stress in Kidney Injury: Insights from Preclinical Models.Biology · 2026Review
- Mitophagy in kidney and lung epithelial cells: molecular mechanisms, crosstalk, and therapeutic interventions.Frontiers in physiology · 2026Review
- Exploring the Mechanism of Shexiang Baoxin Pill in the Treatment of Ischemic Stroke: A Study Integrating Network Pharmacology, Machine Learning, Molecular Docking, and Molecular Dynamics Simulation.BioMed research international · 2026Article
- Macrophage metabolic reprogramming in organ transplantation: mechanisms, transplant outcomes, and therapeutic implications.Frontiers in cellular and infection microbiology · 2026Review
- Ozone protects against ischemia-reperfusion injury: molecular mechanisms.Frontiers in pharmacology · 2026Review
- Hypoxic tumor exosomes suppress macrophage inflammation and ferroptosis via NDUFV2 to enhance bystander tumor radioresistance.Cell death & disease · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Ischemia reperfusion injury (IRI) is commonly seen in surgical procedures involving cardiopulmonary bypass and post-shock reperfusion. Sudden restoration of blood flow after a period of ischemia triggers a rapid accumulation of reactive oxygen species (ROS) and oxidative stress that promote pathological injury. Macrophage-derived inflammatory responses are also thought to contribute to such injury, but how ROS influences tissue macrophages and their elaboration of inflammatory cytokines in IRI remains poorly understood. In this study, we showed that macrophages mobilize mitochondrial adaptations during reoxygenation, including mitochondrial fission and ubiquitin proteasome system (UPS) flux. Furthermore, the transcription factor Nuclear Factor Erythroid 2 Like 1 (NRF1) is rapidly induced during reoxygenation in response to rising levels of ROS. Induction of NRF1 upregulates ubiquitin proteasome system (UPS) and mitophagy pathways to mediate mitochondrial fusion/fission dynamics and dampen ROS production, allowing for alleviation of oxidative stress and the inflammatory response. Conversely, the absence of myeloid NRF1 leads to increased ROS, driving enhanced inflammation and kidney injury in a mouse model of IRI. We thus identify macrophage NRF1 as a master regulator of mitochondrial homeostasis, antioxidant defense, and inflammatory responses in IRI.
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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.