NADPH Oxidases and Mitochondria in Vascular Senescence

Salazar, Gloria

doi:10.3390/ijms19051327

Cited by 133Nitric Oxide and Endothelin EffectsTelomeres, Telomerase, and SenescenceMitochondrial Function and Pathology

NADPH Oxidases and Mitochondria in Vascular Senescence

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Salazar, Gloria·2018·International Journal of Molecular Sciences

DOI 10.3390/ijms19051327PMC PMC5983750

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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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Zinc overload can contribute to increased cellular oxidative stress and senescence through mechanisms possibly related to organelle dysfunction.
“On the other hand, Zn overload can contribute to augment cellular OS and senescence through different mechanisms not yet well-defined, but possibly related to organelles dysfunction [411,427,438].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [438]

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Microvascular NADPH oxidase in health and disease
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NOX4-derived reactive oxygen species limit fibrosis and inhibit proliferation of vascular smooth muscle cells in diabetic atherosclerosis
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Zinc stimulates glucose consumption by modulating the insulin signaling pathway in L6 myotubes: essential roles of Akt–GLUT4, GSK3β and mTOR–S6K1
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“While senescence may protect against the initiation of tumorigenesis, due to lack of proliferation, the development of the SASP may promote proliferation of an established tumor [4,5].”
Background
Metal binding properties of zinc fingers with a naturally altered metal binding site
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Constitutive NADPH Oxidase 4 Activity Resides in the Composition of the B-loop and the Penultimate C Terminus
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Angiotensin II stimulates superoxide production in the thick ascending limb by activating NOX4
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3 of the 149 references couldn’t be matched to a known paper.

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The Role of NADPH Oxidases and Oxidative Stress in Neurodegenerative Disorders
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Cross-Talk between NADPH Oxidase and Mitochondria: Role in ROS Signaling and Angiogenesis
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Roles of Oxidative Stress and Inflammation in Vascular Endothelial Dysfunction-Related Disease
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Protective Role of Polyphenols against Vascular Inflammation, Aging and Cardiovascular Disease
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SQSTM1/p62 and PPARGC1A/PGC-1alpha at the interface of autophagy and vascular senescence
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Glucose Metabolism and Glucose Transporters in Breast Cancer
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Crosstalk Between Oxidative Stress and Endoplasmic Reticulum (ER) Stress in Endothelial Dysfunction and Aberrant Angiogenesis Associated With Diabetes: A Focus on the Protective Roles of Heme Oxygenase (HO)-1
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Endothelial Glycocalyx
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New Dawn for Atherosclerosis: Vascular Endothelial Cell Senescence and Death
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A review on the advances in the extraction methods and structure elucidation of Poria cocos polysaccharide and its pharmacological activities and drug carrier applications
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Frailty as a phenotypic manifestation of underlying oxidative stress
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Authors: Salazar, G.
Affiliations: Florida State University (US)
Corresponding author: Salazar, Gloria
ORCID: Salazar, Gloria
Venue: International Journal of Molecular Sciences
Publisher: MDPI AG
Published: 2018-04-29
Volume: 19
Issue: 5
Pages: 1327
ISSN: 1422-0067 (ISSN-L)
DOI: 10.3390/ijms19051327
PMC: PMC5983750
OpenAlex: W2800217088
Cited by: 133
References: 149
Citations by year: 2026: 5 · 2025: 14 · 2024: 21 · 2023: 14 · 2022: 27 · 2021: 18 · 2020: 17 · 2019: 14 · 2018: 3
FWCI: 1.71
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0/ (vor)
Locations: International Journal of Molecular Sciences (publishedVersion, cc-by)
Europe PMC (PubMed Central) (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: American Heart Association (14GRNT20180028)
Topics: Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords: vascular aging, NADPH oxidase, NOX1, NOX4, mitochondria, oxidative stress, reactive oxygen species, atherosclerosis, PGC-1α, NF-κB, zinc transporters, ZnT3, zinc, angiotensin II, telomere stability, aging, cardiovascular disease, inflammation
MeSH terms: Animals, Blood Vessels, Humans, Mitochondria, Cellular Senescence, Oxidative Stress, NADPH Oxidases, Atherosclerosis

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