The DOI matches its Crossref record; 146 of the 149 references it cites were found in a registry or an index.
NADPH Oxidases and Mitochondria in Vascular Senescence
Open accessAbstract
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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“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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Cites
The senescence-associated secretory phenotype: the dark side of tumor suppression
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
A complex secretory program orchestrated by the inflammasome controls paracrine senescence
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].”
BackgroundSt-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
Sir2 mediates longevity in the fly through a pathway related to calorie restriction
Rogina, B., & Helfand, S. L. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0404184101 · Cited by 1,361
Telomere dysfunction induces metabolic and mitochondrial compromise
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].”
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Items 101–131 of 131
Diabetes mellitus can cause cardiomyopathy disorders by inducing the aging pathway.
Ahmadi, M., Saberianpour, S., Heidarzadeh, M., & Rezaie, J. (2021) · PubMed Central · doi:10.22038/ijbms.2021.54783.12287 · Cited by 4
Peng, S., Chen, Q., Ke, W., & Wu, Y. (2025) · Vascular Health and Risk Management · doi:10.2147/vhrm.s511277 · Cited by 3
“38 Aging, the process through which cells cease multiplying and become dysfunctional, is a result of both inflammatory processes and oxidative stress.”
Wang, F., Hui, S. T. Y., Stappenbeck, F., Kamińska, D., Lusis, A. J., & Parhami, F. (2025) · Cells · doi:10.3390/cells14151191 · Cited by 4
“Oxidative stress, caused by an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, is a known driver of vascular senescence and MASH [34].”
Dong, Y., Zhang, Y., Li, F., Tang, B., Lv, D., Wang, H., & Luo, S. (2023) · Journal of Leukocyte Biology · doi:10.1093/jleuko/qiad116 · Cited by 3
NADPH Oxidase 5 (NOX5) Upregulates MMP-10 Production and Cell Migration in Human Endothelial Cells
Marqués, J., Ainzúa, E., Orbe, J., Martínez-Azcona, M., Martínez‐González, J., & Zalba, G. (2024) · Antioxidants · doi:10.3390/antiox13101199 · Cited by 3
“Collectively, these results allow us to speculate on a possible role of NOX5 in the composition of the vascular ECM, which could lead to the establishment of endothelial dysfunction and the development of complications in cardiovascular diseases.”
BackgroundSivakumar, R., Aravaanan, A. S. K., Mohanakrishnan, V. V., & Kumar, J. (2025) · Current Cardiology Reviews · doi:10.2174/011573403x375709250616134726 · Cited by 2
“…"mitochondrial dysfunction" Chronic systemic inflammation, driven by mitochondrial dysfunction and the senescence-associated secretory phenotype (SASP), disrupts extracellular matrix (ECM) remodeling and increases collagen deposition, promoting vascular stiffness and impairing blood flow [31-35].”
Borghini, A., Palazzo, M., Tonacci, A., Minichilli, F., Wu, H., & Gorini, F. (2026) · Antioxidants · doi:10.3390/antiox15070786 · Cited by 2
“NP treatment downregulates Sirt1, a key stress and energy sensor activated by an increased NAD + /NADH ratio, thereby promoting endothelial dysfunction and NADPH oxidase-dependent ROS production, ultimately contributing to vascular senescence and atherosclerosis development [81–84].”
Che, J., Sun, Y., Wang, F., Feng, Q., 徐翠香, & Li, X. F. (2026) · Antioxidants · doi:10.3390/antiox15070830 · Cited by 3
“Moreover, DNA damage and telomere attrition associated with aging activate p53, thereby inhibiting PGC-1 α production [75,76].”
Fakfum, P., Chuljerm, H., Parklak, W., Roytrakul, S., Phaonakrop, N., Lerttrakarnnon, P., & Kulprachakarn, K. (2024) · Life · doi:10.3390/life14101269 · Cited by 2
Pan, G., Yang, S., Han, X., Wang, X., Kou, L., Xie, J., & Li, C. (2022) · Human & Experimental Toxicology · doi:10.1177/09603271221124099 · Cited by 2
“It is of great importance to clarify the expression and role of NOX in common cardiovascular diseases for the implementation of clinical antioxidant therapy.(9) Among them, NOX is an important source of active oxygen in the body.”
BackgroundImportance of CoQ10-dependent Redox Activity in Aging
López‐Lluch, G. (2021) · Healthy ageing and longevity · doi:10.1007/978-3-030-84965-8_9 · Cited by 3
Thakar, S., Bhattacharyya, R., Katakia, Y. T., Jayakumar, H., Chakraborty, S., Ramakrishnan, S. K., Thakkar, N. P., Dey, S., Chowdhury, S., & Majumder, S. (2025) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2025.144963 · Cited by 1
KOZAK, T., LYKHOVA, O., & Chekhun, V. F. (2025) · Experimental Oncology · doi:10.15407/exp-oncology.2025.01.003 · Cited by 1
“It is NADPH that malignant cells use as a powerful antioxidant maintaining redox homeostasis [42].”
Dexmedetomidine Stimulates Cellular Senescence of Lung Cancer Cells Via NOX5
Zhang, D., Wei, L., Li, Z., Chen, D., Jiang, J., Li, Y., & Wang, F. (2025) · Journal of Biochemical and Molecular Toxicology · doi:10.1002/jbt.70414 · Cited by 2
“NADPH oxidases (NOXs) are reported to participate in the processing of cellular senescence [26].”
Ren, G.-Q., Liu, H.-J., Guo, Y., He, M., Li, J., Li, Z.-X., Jia, C.-H., Liu, T., & (13969), J. Y. (2026) · Molecular Biology Reports · doi:10.1007/s11033-026-11626-z · Cited by 1
“HFD is a well-recognized Vascular aging is a fundamental pathological process in the development of atherosclerosis, involving oxidative stress, mitochondrial dysfunction, and aberrant cell cycle regulation [29].”
Reactive oxygen species-induced reactive oxygen species release in vascular signaling and disease
Kim, Y.-M., & Ushio‐Fukai, M. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-816196-8.00019-9 · Cited by 1
Sazonova, M. A., Синёв, В. В., Ryzhkova, A. I., Sazonova, M. D., Дорощук, Н. А., Kirichenko, T. V., Карагодин, В. П., Орехов, А. Н., & Sobenin, I. A. (2020) · Zhurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia» · doi:10.25557/0031-2991.2020.04.140-147 · Cited by 1
Yu, B., Shen, K., Qin, H., Liu, X., Wang, L., He, S., Zhao, X., Yang, J., & Wang, S. (2022) · Research Square · doi:10.21203/rs.3.rs-1750917/v1 · Cited by 1
Ren, C., & Li, M. (2022) · Research Square · doi:10.21203/rs.3.rs-1456635/v1
Coenzyme Q as an Antiaging Strategy
López‐Lluch, G. (2023) · Springer eBooks · doi:10.1007/978-981-19-7443-4_2
Thakar, S., Bhattacharyya, R., Katakia, Y. T., Chakraborty, S., Ramakrishnan, S., Thakkar, N. P., Dey, S., Chowdhury, S., & Majumder, S. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.05.12.540614
Zang, Z., Wu, X., Ma, D., Xia, X., He, X., Chen, X., & Li, Z. (2023) · Blood Purification · doi:10.1159/000530773
α-Mangostin protects endothelial cell against H2O2-induced senescence via p38/Sirt1/MnSOD pathway
Jittiporn, K., Samer, J., & Thitiwuthikiat, P. (2024) · Journal of Applied Pharmaceutical Science · doi:10.7324/japs.2024.161374
邹, 志. (2024) · Advances in Clinical Medicine · doi:10.12677/acm.2024.1441187
Fang, Z., Wang, L., Wang, Y., Ma, Y., Fang, Y., Zhang, W., Cao, R., Zhang, Y., Li, H., Chen, S., et al. (2024) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2024.112021
Cytokine and Oxidative Stress Imbalances in Relation to Complex Coronary Lesions in Elderly Patients
Li, X., Zhao, Y., Zhou, H., Hu, Y., Chen, Y., & Guo, D. (2025) · Current Vascular Pharmacology · doi:10.2174/0115701611323165250211045917
Zhang, F., Liao, Y., Yang, P., & Guo, J. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1850084
“Mitochondrial dysfunction and ROS production not only directly activate NF-k B but also enhance the SASP effect through metabolic reprogramming, further exacerbating the in fl ammatory response (55).”
Emerging links between TLR4 signaling and ferroptosis in heart failure
Wang, C., Huang, X., Zhang, Z., Hu, Y., Lin, D., & Huang, S. (2026) · Frontiers in Pharmacology · doi:10.3389/fphar.2026.1909522
“Subsequently, NOX1 utilizes two heme molecules to transfer an electron from NADPH on the cytoplasmic side of the phagosome membrane to an oxygen molecule on the lumen side, promoting the generation of superoxide anions within the phagosome lumen (Salazar, 2018; Parascandolo and Laukkanen, 2019).”
Metadata
- 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)
- 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
- 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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