ArticleAntioxidants & redox signaling2014
Molecular mechanisms of the crosstalk between mitochondria and NADPH oxidase through reactive oxygen species-studies in white blood cells and in animal models.
Article in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 2 of them syntheses that pooled it.
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
133 citing papers in PubMed, 2 syntheses or guidelines pooled it, 243 citations in OpenAlex.
- Comprehensive analysis of regulated cell death pathways: intrinsic disorder, protein-protein interactions, and cross-pathway communication.Apoptosis : an international journal on programmed cell death · 2025Pooled it
- Antioxidants Supplementation During Exercise: Friends or Enemies for Cardiovascular Homeostasis?Journal of cardiovascular translational research · 2023Pooled it
- Blocking mitochondrial cyclophilin D ameliorates TSH-impaired defensive barrier of artery.Redox biology · 2018Trial
- A review on applying immunological methods in animal research.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Review
- The Role of Oral Pathobionts' Outer Membrane Vesicles in Cancer Pathology and Therapeutic Development.Cells · 2026Review
- Fabry Disease: A Focus on the Role of Oxidative Stress.Antioxidants (Basel, Switzerland) · 2026Review
- Decoding mitochondrial signaling: neutrophil-tumor cell crosstalk in orchestrating cancer progression.Journal of translational medicine · 2026Review
- Succinate Dehydrogenase Subunit A (SDHA) Mediated Microglia Extracellular Traps Formation Participating in Cerebral Ischemic Reperfusion Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Crosstalk Between Metabolic Biomarkers and Pulse Wave Analysis in Hypertensive Patients.Biomedicines · 2025Article
- CD40-TRAF6 inhibition suppresses cardiovascular inflammation, oxidative stress and functional complications in a mouse model of arterial hypertension.Redox biology · 2025Article
- Endothelial Dysfunction: Redox Imbalance, NLRP3 Inflammasome, and Inflammatory Responses in Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- The Role of mtDNA Mutations in Atherosclerosis: The Influence of Mitochondrial Dysfunction on Macrophage Polarization.International journal of molecular sciences · 2025Review
- Short-term exposure of 2.4 GHz electromagnetic radiation on cellular ROS generation and apoptosis in SH-SY5Y cell line and impact on developing chick embryo brain tissue.Molecular biology reports · 2025Article
- Reactive oxygen species in hypertension.Nature reviews. Cardiology · 2025Review
- Emerging insights into the pathogenesis and therapeutic strategies for vascular endothelial injury-associated diseases: focus on mitochondrial dysfunction.Angiogenesis · 2024Review
- The Role of Oxidative Stress as a Mechanism in the Pathogenesis of Acute Heart Failure in Acute Kidney Injury.Diagnostics (Basel, Switzerland) · 2024Review
- Antioxidant-related enzymes and peptides as biomarkers of metallic nanoparticles (eco)toxicity in the aquatic environment.Chemosphere · 2024Review
- Role of inflammatory signaling pathways involving the CD40-CD40L-TRAF cascade in diabetes and hypertension-insights from animal and human studies.Basic research in cardiology · 2024Article
- Mitochondrial calcium in cardiac ischemia/reperfusion injury and cardioprotection.Basic research in cardiology · 2024Review
- Bacteria-organelle communication in physiology and disease.The Journal of cell biology · 2024Review
73 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsOxidative stress is involved in the development of cardiovascular disease. There is a growing body of evidence for a crosstalk between different enzymatic sources of oxidative stress. With the present study, we sought to determine the underlying crosstalk mechanisms, the role of the mitochondrial permeability transition pore (mPTP), and its link to endothelial dysfunction.
resultsNADPH oxidase (Nox) activation (oxidative burst and translocation of cytosolic Nox subunits) was observed in response to mitochondrial reactive oxygen species (mtROS) formation in human leukocytes. In vitro, mtROS-induced Nox activation was prevented by inhibitors of the mPTP, protein kinase C, tyrosine kinase cSrc, Nox itself, or an intracellular calcium chelator and was absent in leukocytes with p47phox deficiency (regulates Nox2) or with cyclophilin D deficiency (regulates mPTP). In contrast, the crosstalk in leukocytes was amplified by mitochondrial superoxide dismutase (type 2) (MnSOD(+/-)) deficiency. In vivo, increases in blood pressure, degree of endothelial dysfunction, endothelial nitric oxide synthase (eNOS) dysregulation/uncoupling (e.g., eNOS S-glutathionylation) or Nox activity, p47phox phosphorylation in response to angiotensin-II (AT-II) in vivo treatment, or the aging process were more pronounced in MnSOD(+/-) mice as compared with untreated controls and improved by mPTP inhibition by cyclophilin D deficiency or sanglifehrin A therapy. INNOVATION: These results provide new mechanistic insights into what extent mtROS trigger Nox activation in phagocytes and cardiovascular tissue, leading to endothelial dysfunction.
conclusionsOur data show that mtROS trigger the activation of phagocytic and cardiovascular NADPH oxidases, which may have fundamental implications for immune cell activation and development of AT-II-induced hypertension.
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.