ReviewInternational journal of molecular sciences2018
NADPH Oxidases and Mitochondria in Vascular Senescence.
Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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.
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Who cites it
73 citing papers in PubMed.
- NADPH Oxidase Overactivity Underlies Telomere Shortening in Human Atherosclerosis.International journal of molecular sciences · 2020Trial
- Mitochondrial Quality Control in Age-Related Diseases: From Molecular Architecture to Precision Therapeutics.Antioxidants (Basel, Switzerland) · 2026Review
- Environmental Exposure to Micro- and Nanoplastics: Linking Cardiovascular Disease and Cancer Through Shared Biological Pathways-A Critical Review.Antioxidants (Basel, Switzerland) · 2026Review
- Mitochondrial-Derived Peptides as Therapeutics and Biomarkers for Combating Vascular Aging and Associated Cardiovascular Diseases.Current cardiology reviews · 2026Review
- Smooth Muscle LRRC8A Knockout Preserves Vascular Function in Ang II Hypertension.Hypertension (Dallas, Tex. : 1979) · 2026Article
- SASP-mediated cellular senescence following myocardial infarction: from spatiotemporal immune regulation to therapeutic strategies.Frontiers in immunology · 2026Review
- Exosomes in aging and age-related disorders: mechanisms, therapeutic potentials, and challenges.Journal of translational medicine · 2025Review
- Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025Review
- Role of Matricellular Proteins in Endothelial Cell Inflammation and Atherosclerosis.Antioxidants (Basel, Switzerland) · 2025Review
- Article
- Radiation-Induced Cardiac Remodeling: Mechanisms and Therapeutic Approaches.Cardiovascular toxicology · 2025Review
- Predicting In-Hospital Mortality in Myocardial Infarction: A Nomogram-Based Retrospective Analysis of the MIMIC-IV Database.Vascular health and risk management · 2025Article
- Cytokine and Oxidative Stress Imbalances in Relation to Complex Coronary Lesions in Elderly Patients.Current vascular pharmacology · 2025Article
- Inhibition of the RXRA-PPARα-FABP4 signaling pathway alleviates vascular cellular aging by an SGLT2 inhibitor in an atherosclerotic mice model.Science China. Life sciences · 2024Article
- Article
- Sexual Dimorphism in Impairment of Acetylcholine-Mediated Vasorelaxation in Zucker Diabetic Fatty (ZDF) Rat Aorta: A Monogenic Model of Obesity-Induced Type 2 Diabetes.International journal of molecular sciences · 2024Article
- Plasma Proteomics of Type 2 Diabetes, Hypertension, and Co-Existing Diabetes/Hypertension in Thai Adults.Life (Basel, Switzerland) · 2024Article
- NADPH Oxidase 5 (NOX5) Upregulates MMP-10 Production and Cell Migration in Human Endothelial Cells.Antioxidants (Basel, Switzerland) · 2024Article
- Factor XII signaling via uPAR-integrin β1 axis promotes tubular senescence in diabetic kidney disease.Nature communications · 2024Article
- Vascular Aging in Ischemic Stroke.Journal of the American Heart Association · 2024Review
13 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
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is the major risk factor in the development of cardiovascular diseases (CVDs), including hypertension, atherosclerosis, and myocardial infarction. Oxidative stress caused by overproduction of reactive oxygen species (ROS) and/or by reduced expression of antioxidant enzymes is a major contributor to the progression of vascular senescence, pathologic remodeling of the vascular wall, and disease. Both oxidative stress and inflammation promote the development of senescence, a process by which cells stop proliferating and become dysfunctional. This review focuses on the role of the mitochondria and the nicotinamide adenine dinucleotide phosphate (NADPH) oxidases Nox1 and Nox4 in vascular senescence, and their contribution to the development of atherosclerosis. Recent findings are reviewed, supporting a critical role of the mitochondrial regulator peroxisome proliferator-activated receptor gamma (PPARγ) coactivator-1α (PGC-1α), the inflammatory gene nuclear factor κB (NF-κB), zinc, the zinc transporters (ZnTs) ZnT3 and ZnT10, and angiotensin II (Ang II) in mitochondrial function, and their role in telomere stability, which provides new mechanistic insights into a previously proposed unified theory of aging.
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Registered trials
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