The DOI matches its Crossref record; 63 of the 63 references it cites were found in a registry or an index.
The role of reactive oxygen species in the pathophysiology of cardiovascular diseases and the clinical significance of myocardial redox
Open accessAbstract
Acute and chronic excessive intracellular increase of reactive oxygen species (ROS) is involved in the development and progression of cardiovascular diseases. ROS are by-products of various oxidative physiological and biochemical processes. Sources of ROS are mitochondrial respiration, NADH/NADPH oxidase, xanthine oxidoreductase or the uncoupling of nitric oxide synthase (NOS) in vascular cells. ROS mediate various signaling pathways that underlie cardiovascular pathophysiology. The delicate equilibrium between free-radical generation and antioxidant defense is altered in favor of the former, thus leading to redox imbalance, oxidative stress, and increased cellular injury. An understanding of the pathophysiological mechanisms mediated by oxidative stress is crucial to the prevention and treatment of cardiovascular diseases.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Reactive oxygen species (ROS) homeostasis and redox regulation in cellular signaling
Ray, P. D., Huang, B.-W., & Tsuji, Y. (2012) · Cellular Signalling · doi:10.1016/j.cellsig.2012.01.008 · Cited by 4,373
(2013) · European Heart Journal · doi:10.1093/eurheartj/eht108 · Cited by 1,955
Berry, C. E., & Hare, J. M. (2004) · The Journal of Physiology · doi:10.1113/jphysiol.2003.055913 · Cited by 927
(2014) · Revista Española de Cardiología (English Edition) · doi:10.1016/j.rec.2013.10.013 · Cited by 609
Dai, D.-F., Johnson, S. C., Villarin, J. J., Chin, M. T., Nieves-Cintrón, M., Chen, T., Marcinek, D. J., Dorn, G. W., Kang, Y. J., Prolla, T. A., et al. (2011) · Circulation Research · doi:10.1161/circresaha.110.232306 · Cited by 527
Activation of NADPH Oxidase During Progression of Cardiac Hypertrophy to Failure
Li, J.-M., Gall, N. P., Grieve, D. J., Chen, M., & Shah, A. M. (2002) · Hypertension · doi:10.1161/01.hyp.0000032031.30374.32 · Cited by 516
Role of oxidative stress in transition of hypertrophy to heart failure
Dhalla, A. K., Hill, M. F., & Singal, P. K. (1996) · Journal of the American College of Cardiology · doi:10.1016/0735-1097(96)00140-4 · Cited by 427
Maack, C., Kartes, T., Kilter, H., Schäfers, H.-J., Nickenig, G., Böhm, M., & Laufs, U. (2003) · Circulation · doi:10.1161/01.cir.0000091084.46500.bb · Cited by 423
Kim, Y. M., Guzik, T. J., Zhang, Y. H., Zhang, M. H., Kattach, H., Ratnatunga, C., Pillai, R., Channon, K. M., & Casadei, B. (2005) · Circulation Research · doi:10.1161/01.res.0000183735.09871.61 · Cited by 405
Dudley, S. C., Hoch, N. E., McCann, L. A., Honeycutt, C., Diamandopoulos, L., Fukai, T., Harrison, D. G., Dikalov, S. I., & Langberg, J. (2005) · Circulation · doi:10.1161/circulationaha.105.538108 · Cited by 374
Cited by
ROS and diseases: role in metabolism and energy supply
Yang, S., & Lian, G. (2020) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-019-03667-9 · Cited by 658
Theranostic Fluorescent Probes
Sharma, A., Verwilst, P., Li, M., Ma, D., Singh, N., Yoo, J., Kim, Y., Yang, Y., Zhu, J.-H., Huang, H., et al. (2024) · Chemical Reviews · doi:10.1021/acs.chemrev.3c00778 · Cited by 499
Jungert, A., & Frank, J. (2021) · Antioxidants · doi:10.3390/antiox10030448 · Cited by 9
Biocompatibility and toxicity challenges of nanomaterials
Yaşayan, G., Alarcin, E., Avci-Adali, M., Ipek, T. C., Nejati, O., Özcan-Bülbül, E., Karslı, S., Bal-Öztürk, A., & Mostafavi, E. (2024) · Functionalized Nanomaterials for Cancer Research · doi:10.1016/b978-0-443-15518-5.00019-7 · Cited by 8
Metadata
- Authors
- Moris, D., Spartalis, M., Spartalis, E., Karachaliou, G.-S., Karaolanis, G. I., Tsourouflis, G., Tsilimigras, D. I., Tzatzaki, E., & Theocharis, S.
- Venue
- Annals of Translational Medicine
- Publisher
- AME Publishing Company
- Published
- 2017-08
- Volume
- 5
- Issue
- 16
- Pages
- 326-326
- ISSN
- 2305-5839 (ISSN-L)
- 2305-5847
- OpenAlex
- W2744282338
- Cited by
- 308
- References
- 63
- FWCI
- 10.30
- Type
- journal article
- Language
- en
- Open access
- hybrid
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: The role of reactive oxygen species in the pathophysiology of cardiovascular diseases and the clinical significance of myocardial redox. https://app.cochat.ai/papers/10.21037/atm.2017.06.27
- The paper
- Moris, D., Spartalis, M., Spartalis, E., Karachaliou, G.-S., Karaolanis, G. I., Tsourouflis, G., Tsilimigras, D. I., Tzatzaki, E., & Theocharis, S. (2017). The role of reactive oxygen species in the pathophysiology of cardiovascular diseases and the clinical significance of myocardial redox. Annals of Translational Medicine. https://doi.org/10.21037/atm.2017.06.27
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.