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

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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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Figure 1 Molecular pathways involved in senescence. Persistent DNA damage response (DDR) activates the ATM/p53/p21 pathway to stop the cell cycle, while preventing lysosomal acidification that inhibits autophagy, and activating NF-κB that induces senescence associated secretory phenotype (SASP). mTOR and reactive oxygen species (ROS) can induce senescence by DDR-independent mechanisms through the p38MAPK/NF-κB/SASP pathway. mTOR can also inhibit autophagy by a NF-κB-independent mechanism to induce senescence. Altogether, cell cycle arrest, reduced autophagy, and secretion of SASP components mediate vascular dysfunction and accelerated aging.CC BY · PubMed Central

Figure 2 The role of Ang II in vascular senescence. Ang II binding to AT1R activates signal transduction pathways, including phosphorylation of p38MAPK, a driver of the SASP, and Akt, a negative regulator of PGC-1α function. Akt phosphorylates PGC-1α, increasing its acetylation, which reduces the binding of PGC-1α/FoxO1 (forkhead box O 1) to catalase and Sirt1(silence information regulator 2-like 1) promoters, reducing the expression of these target genes. Reduced Sirt1 expression further increases PGC-1α and FoxO1 acetylation, creating a negative feedback loop. Ang II also increases cytosolic zinc levels, leading to mitochondrial zinc accumulation that causes mitochondrial dysfunction and mitochondrial ROS (MitoROS) production that mediates NF-κB activation and Nox1 expression. NF-κB drives the SASP, and also mediates Nox4 upregulation and oxidative stress. Sirt1 inhibits senescence by deacetylating NF-κB, PGC-1α and FoxO1, thus improving mitochondrial function and the antioxidant capacity, while zinc induces senescence by causing mitochondrial dysfunction, increasing Nox1 and reducing catalase expression. SASP stimulates senescence in bystander cells.CC BY · PubMed Central

Figure 3 PGC-1α and Nox1 in telomere and mitochondrial dysfunction during aging. Telomere dysfunction induces mitochondrial dysfunction through the p53-dependent downregulation of PGC-1α. Dysfunctional mitochondria produce mitochondrial ROS (MitoROS) that activates NF-κB-dependent upregulation of Nox1, causing telomere attrition and replicative senescence. Ang II induces senescence by inhibiting PGC-1α function, while zinc overload causes senescence by increasing MitoROS and Nox1 expression. In conditions of stress, Nox4 localizes in the mitochondria, also contributing to MitoROS production.CC BY · PubMed Central

Figure 4 Proposed role of Nox1 and Nox4 in senescence. Hydrogen peroxide associated with basal Nox4 activity in physiological conditions protects from senescence, while overproduction of hydrogen peroxide during aging and stress conditions may promote senescence. Binding of zinc to the E-loop of Nox4 or oxidation of cysteine residues in the E-loop in response to stress conditions by overexpression of Nox1 could change the function of Nox4. Altered production of superoxide by Nox4 could mediate senescence in conditions of stress. Red arrows indicate increased expression.CC BY · PubMed Central

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Coppé, J.-P., Desprez, P.-Y., Krtolica, A., & Campisi, J. (2010) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-121808-102144 · Cited by 5,206
Stress-dependent regulation of FOXO transcription factors by the SIRT1 deacetylase
Brunet, A., Sweeney, L. B., Sturgill, J. F., Chua, K. F., Greer, P. L., Lin, Y., Tran, H., Ross, S. E., Mostoslavsky, R., Cohen, H. Y., et al. (2004) · Science · doi:10.1126/science.1094637 · Cited by 3,239
NAD(P)H Oxidase: Role in Cardiovascular Biology and Disease
Griendling, K. K., Sorescu, D., & Ushio-Fukai, M. (2000) · Circulation Research · doi:10.1161/01.res.86.5.494 · Cited by 2,886
Cellular senescence in aging and age-related disease: from mechanisms to therapy
Childs, B. G., Durik, M., Baker, D. J., & van Deursen, J. M. (2015) · Nature Medicine · doi:10.1038/nm.4000 · Cited by 2,363
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Acosta, J. C., Banito, A., Wuestefeld, T., Georgilis, A., Janich, P., Morton, J. P., Athineos, D., Kang, T.-W., Lasitschka, F., Andrulis, M., et al. (2013) · Nature Cell Biology · doi:10.1038/ncb2784 · Cited by 2,278 · cited 1×
“In many cell types, the SASP is driven by IL1α [10] and by IL1β [13].”
Background
Suppression of Reactive Oxygen Species and Neurodegeneration by the PGC-1 Transcriptional Coactivators
St-Pierre, J., Drori, S., Uldry, M., Silvaggi, J. M., Rhee, J., Jäger, S., Handschin, C., Zheng, K., Lin, J., Yang, W., et al. (2006) · Cell · doi:10.1016/j.cell.2006.09.024 · Cited by 2,233
Cellular senescence and the senescent secretory phenotype: therapeutic opportunities
Tchkonia, T., Zhu, Y., van Deursen, J., Campisi, J., & Kirkland, J. L. (2013) · Journal of Clinical Investigation · doi:10.1172/jci64098 · Cited by 1,774
Increased dosage of a sir-2 gene extends lifespan in Caenorhabditis elegans
Tissenbaum, H. A., & Guarente, L. (2001) · Nature · doi:10.1038/35065638 · Cited by 1,603
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Rogina, B., & Helfand, S. L. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0404184101 · Cited by 1,361
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Sahin, E., Colla, S., Liesa, M., Moslehi, J., Müller, F. L., Guo, M., Cooper, M., Kotton, D., Fabian, A. J., Walkey, C., et al. (2011) · Nature · doi:10.1038/nature09787 · Cited by 1,319 · cited 1×
“demonstrated that telomere dysfunction causes mitochondrial dysfunction by p53-dependent downregulation of PGC-1α and PGC-1β, leading to mitochondrial dysfunction and increased ROS production [83].”
Background

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Background
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Background
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Sakurada, R., Odagiri, K., Hakamata, A., Kamiya, C., Wei, J., & Watanabe, H. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20071644 · Cited by 27
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Elwakiel, A., Gupta, D., Rana, R., Manoharan, J., Al‐Dabet, M. M., Ambreen, S., Fatima, S., Zimmermann, S., Mathew, A., Li, Z., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-52214-8 · Cited by 27
“Rac1 activates NADPH oxidases (NOXs), increasing ROS generation, DNA damage and senescence 97,98 .”
Development and validation of a prognostic nomogram for myocardial infarction patients in intensive care units: a retrospective cohort study
Guo, Q., Wu, M., Li, H., Ouyang, H., Sun, R., Wang, J., Liu, Z., Wang, J., & Zhang, Y. (2020) · BMJ Open · doi:10.1136/bmjopen-2020-040291 · Cited by 25
Inhibition of the RXRA-PPARα-FABP4 signaling pathway alleviates vascular cellular aging by an SGLT2 inhibitor in an atherosclerotic mice model
Zhang, W., Wang, L., Wang, Y., Fang, Y., Cao, R., Fang, Z., Han, D. G., Huang, X., Gu, Z., Zhang, Y., et al. (2024) · Science China Life Sciences · doi:10.1007/s11427-024-2602-7 · Cited by 22
“Previous research has shown that the generation of ROS and a decrease in antioxidant levels can promote cellular aging and induce vascular aging (Salazar, 2018).”
Epigenetically regulated inflammation in vascular senescence and renal progression of chronic kidney disease
Chao, C., Kuo, F.-C., & Lin, S. (2022) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2022.09.012 · Cited by 22
Myricetin Alleviates Silica-Mediated Lung Fibrosis via PPARγ–PGC-1α Loop and Suppressing Mitochondrial Senescence in Epithelial Cells
Xie, W., Deng, L., Zhang, X., Huang, X., Ding, J., Liu, W. Q., & Tang, S. (2024) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.4c04887 · Cited by 20
Recurrent Hypoglycemia Impaired Vascular Function in Advanced T2DM Rats by Inducing Pyroptosis
Luo, M., Hu, Y., Lv, D., Xie, L., Yang, S., Zuo, D., Xue, Y., & He, A. (2022) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2022/7812407 · Cited by 20
“NADPH oxidase (NOX) 2 and 4 are key enzymes involved in electron transfer in the cell membrane and are sources of ROS in the cardiovascular sys-tem [36, 37].”
Sirt7 protects against vascular calcification via modulation of reactive oxygen species and senescence of vascular smooth muscle cells
Yu, H., Xie, Y., Lan, L., Ma, S., Mok, S. W. F., Wong, I. N., Wang, Y., Zhong, G., Yuan, L., Zhao, H., et al. (2024) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2024.07.021 · Cited by 20
“Oxidative stress resulting from overproduction of reactive oxygen species (ROS) and/or by reduced expression of antioxidant enzymes is a major stimulus for vascular cell senescence [14].”
Background
Research progress on the interaction between circadian clock and early vascular aging
Chen, Z., Xiong, Z., & Liu, X. (2021) · Experimental Gerontology · doi:10.1016/j.exger.2021.111241 · Cited by 19
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Wang, D., Wu, J. P., Le, S., Wang, H., Luo, J., Li, R., Chen, X., Song, Y. M., Wu, L., Ye, P., et al. (2022) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2022.175361 · Cited by 18
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Lu, P., Zhang, T., Ren, Y., Rao, H., Lei, J., Zhao, G., Wang, M., Gong, D., & Cao, Z. (2023) · Natural Product Communications · doi:10.1177/1934578x231171521 · Cited by 19
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Background
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Inflachromene inhibits intimal hyperplasia through the HMGB1/2- regulated TLR4-NF-κB pathway
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Dapagliflozin ameliorates myocardial infarction injury through AMPKα-dependent regulation of oxidative stress and apoptosis
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“NADPH oxidase (NOX) 2 and 4 are key enzymes involved in electron transfer in cell membranes and contribute to oxidative stress under pathological environments [21 – 23].”
Background
Photobiomodulation and estrogen stabilize mitochondrial membrane potential in angiotensin– II challenged porcine aortic smooth muscle cells
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“Many of the upregulated genes are closely related to the molecular profile of senescent cells and to biological programs of response to cell damage, release of pro-inflammatory factors and generation reactive oxygen species (ROS), among others (Zhang et al., 2019; Kalamakis et al., 2019; Kiss et al., 2020).”
BackgroundInfluential
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Li, S., Cao, C., Huang, Z., Tang, D., Chen, J., Wang, A., & He, Q. (2022) · Oral Diseases · doi:10.1111/odi.14404 · Cited by 13
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“An in-depth study of oxidative homeostasis in blood vessels has shown that the alteration of oxidation homeostasis in the vascular system contributes to the occurrence and development of atherosclerosis, drawing more attention (Salazar, 2018; Marchio et al., 2019).”
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Resveratrol alleviates Ang II-induced vascular smooth muscle cell senescence by upregulating E2F1/SOD2 axis
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Background
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“216 , 217”
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Background
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“One major source of cellular stress is superoxide, which is primarily generated in the mitochondria and by the NOX family [44].”
Background
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“2 ER stress after exposure of cardiomyocytes to IR and subsequent consequences in the heart cells, including cardiomyocytes, endothelial cells, and fibroblasts [86, 87].”
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Liu, X., Jin, Y., Li, Z., Zhao, H.-S., Zhou, X., Zhu, Y., Gu, Y., Zhang, L., Zhang, Y., He, P., et al. (2025) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2025.120525 · Cited by 7
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“For example, NAD(P)H oxidases [40,41], lipoxygenases [42], and increased labile iron [43] have been shown to drive senescence.”
Background
KLF4 inhibited the senescence-associated secretory phenotype in ox-LDL-treated endothelial cells via PDGFRA/NAMPT/mitochondrial ROS
Ding, H., Tong, J., Lin, H., Ping, F., Yao, T., Ye, Z., Chu, J., Yuan, D., Wang, K., Liu, X., et al. (2024) · Aging · doi:10.18632/aging.205805 · Cited by 6
“An increasing number of studies have found that reactive oxygen species (ROS) may be the major inducer of vascular senescence, and the NAD + /mitochondrial ROS (MitoROS) pathway seems to be the most important pathway for ROS production [38].”
Background
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“Similarly, in various cell types and tissues, NOX4-induced senescence contributes to the development of CVDs [125,126].”
Detection of Protein Aggregation and Proteotoxicity Induced by Angiotensin II in Vascular Smooth Muscle Cells
Cicalese, S. M., Okuno, K., & Eguchi, S. (2020) · Journal of Cardiovascular Pharmacology · doi:10.1097/fjc.0000000000000934 · Cited by 5
Deficiency of NARFL increases transcription of NADPH oxidases and ROS production impairing the function of endothelial cells
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“Aging also leads to the inhibition of clathrin-mediated integrin endocytosis, which generates abnormal focal adhesions that activate Rac and ROS production and induce cellular senescence through the p16Ink4a-pRb pathway (142, 153, 154).”
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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 (medical) › Nitric Oxide and Endothelin Effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › 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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NADPH Oxidases and Mitochondria in Vascular Senescence

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