ReviewFree radical biology & medicine2011
Cross talk between mitochondria and NADPH oxidases.
Review in Free radical biology & medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 432 papers.
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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.
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Who cites it
432 citing papers in PubMed.
- Atrial nitroso-redox balance and refractoriness following on-pump cardiac surgery: a randomized trial of atorvastatin.Cardiovascular research · 2022Trial
- Mitochondrial dysfunction and oxidative stress in OSAHS and associated comorbidities: Mechanism and potential targeted therapeutic strategies.Redox biology · 2026Review
- CYP2D6 as an Emerging Endogenous Oxidative Stress Modulator in Cardiovascular Disease: Genetic, Pharmacological, and Redox Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
- Hedgehog/GLI Signaling at the Interface of Sterol Metabolism, Mitochondrial ROS Signaling and Cellular Plasticity.Antioxidants (Basel, Switzerland) · 2026Review
- Sex-dependent differences in mitochondrial protein acetylation in metabolic condition, oxidative stress, vascular dysfunction, hypertension, and cardiovascular disease.Clinical science (London, England : 1979) · 2026Review
- Angiotensin signaling is essential for stress erythropoiesis but causes retention of dysfunctional mitochondria in RBCs.JCI insight · 2026Article
- A Redox Amplification Interface Linking Mitochondrial Dysfunction, Immune-Derived Oxidants, and Biomaterial Electrochemistry in Chronic Inflammation.International journal of molecular sciences · 2026Review
- Verification of quantum biological predictions for weak magnetic field effects on superoxide in planarians.PNAS nexus · 2026Article
- LRRK2 I1371V Mutation Drives Astrocytic Glucose Metabolism Failure and Induces Integrated ER-Mitochondria-Lysosome Dysfunction in Parkinson's Disease.International journal of molecular sciences · 2026Article
- ROS-SUMO Crosstalk in Oxidative Stress: Disease Mechanisms and Reproductive Health.Antioxidants (Basel, Switzerland) · 2026Review
- Phagosome maturation during fungal infection.Current opinion in microbiology · 2026Review
- The AMPK/NRF2/FOXO Axis in CKD-Molecular and Clinical Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
- Metformin induces ferroptosis associated with lipidomic remodeling in AML.Blood advances · 2026Article
- Mitochondrial dysfunction in hypertension: mechanistic pathways and therapeutic implications.Functional & integrative genomics · 2026Review
- Prenatal Alcohol Exposure and Mitochondrial Function in the Brain.Advances in experimental medicine and biology · 2026Review
- Dietary bioactive compounds targeting insulin resistance: mechanisms and preventive potential.Frontiers in nutrition · 2026Review
- Increased Urinary Albumin Excretion But Less Damaged Renal Tubular Structures in Mice with Genetically DecreasedInnovation discovery · 2026Article
- Oxidative stress and endoplasmic reticulum stress in acute kidney injury: mechanistic crosstalk and therapeutic modulation.Frontiers in medicine · 2026Review
- Metabolic Control of Immunity-Unveiling Neutrophil Mechanisms.Advances in experimental medicine and biology · 2026Review
- Skeletal muscle knockout of NAD(P)H oxidase 2 delays the development of isotonic diaphragm fatigue in mice.Free radical biology & medicine · 2025Article
372 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
Reactive oxygen species (ROS) play an important role in physiological and pathological processes. In recent years, a feed-forward regulation of the ROS sources has been reported. The interactions between the main cellular sources of ROS, such as mitochondria and NADPH oxidases, however, remain obscure. This work summarizes the latest findings on the role of cross talk between mitochondria and NADPH oxidases in pathophysiological processes. Mitochondria have the highest levels of antioxidants in the cell and play an important role in the maintenance of cellular redox status, thereby acting as an ROS and redox sink and limiting NADPH oxidase activity. Mitochondria, however, are not only a target for ROS produced by NADPH oxidase but also a significant source of ROS, which under certain conditions may stimulate NADPH oxidases. This cross talk between mitochondria and NADPH oxidases, therefore, may represent a feed-forward vicious cycle of ROS production, which can be pharmacologically targeted under conditions of oxidative stress. It has been demonstrated that mitochondria-targeted antioxidants break this vicious cycle, inhibiting ROS production by mitochondria and reducing NADPH oxidase activity. This may provide a novel strategy for treatment of many pathological conditions including aging, atherosclerosis, diabetes, hypertension, and degenerative neurological disorders in which mitochondrial oxidative stress seems to play a role. It is conceivable that the use of mitochondria-targeted treatments would be effective in these conditions.
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