The DOI matches its Crossref record; 20 of the 20 references it cites were found in a registry or an index.
Redox Signaling in Cardiac Physiology and Pathology
Abstract
Redox signaling refers to the specific and usually reversible oxidation/reduction modification of molecules involved in cellular signaling pathways. In the heart, redox signaling regulates several physiological processes (eg, excitation-contraction coupling) and is involved in a wide variety of pathophysiological and homoeostatic or stress response pathways. Reactive oxygen species involved in cardiac redox signaling may derive from many sources, but NADPH oxidases, as dedicated sources of signaling reactive oxygen species, seem to be especially important. An increasing number of specific posttranslational oxidative modifications involved in cardiac redox signaling are being defined, along with the reactive oxygen species sources that are involved. Here, we review current knowledge on the molecular targets of signaling reactive oxygen species in cardiac cells and their involvement in cardiac physiopathology. Advances in this field may allow the development of targeted therapeutic strategies for conditions such as heart failure as opposed to the general antioxidant approaches that have failed to date.
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
The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology
Bedard, K., & Krause, K.-H. (2007) · Physiological Reviews · doi:10.1152/physrev.00044.2005 · Cited by 6,989
Mitochondrial reactive oxygen species trigger hypoxia-induced transcription
Chandel, N. S., Maltepe, E., Goldwasser, E., Mathieu, C. E., Simon, M. C., & Schumacker, P. T. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.20.11715 · Cited by 1,926
Reactive Oxygen Species (Ros-Induced) Ros Release
Zorov, D. B., Filburn, C. R., Klotz, L.-O., Zweier, J. L., & Sollott, S. J. (2000) · The Journal of Experimental Medicine · doi:10.1084/jem.192.7.1001 · Cited by 1,412
Redox regulation of protein tyrosine phosphatase 1B involves a sulphenyl-amide intermediate
Salmeen, A., Andersen, J. N., Myers, M. P., Meng, T.-C., Hinks, J. A., Tonks, N. K., & Barford, D. (2003) · Nature · doi:10.1038/nature01680 · Cited by 951
Combating oxidative stress in vascular disease: NADPH oxidases as therapeutic targets
Drummond, G. R., Selemidis, S., Griendling, K. K., & Sobey, C. G. (2011) · Nature Reviews Drug Discovery · doi:10.1038/nrd3403 · Cited by 899
Bardoxolone Methyl and Kidney Function in CKD with Type 2 Diabetes
Pergola, P. E., Raskin, P., Toto, R. D., Meyer, C. J., Huff, J. W., Grossman, E. B., Krauth, M., Ruiz, S., Audhya, P., Christ-Schmidt, H., et al. (2011) · New England Journal of Medicine · doi:10.1056/nejmoa1105351 · Cited by 890
Cucoranu, I., Clempus, R., Dikalova, A., Phelan, P. J., Ariyan, S., Dikalov, S., & Sorescu, D. (2005) · Circulation Research · doi:10.1161/01.res.0000187457.24338.3d · Cited by 786
NADPH oxidase 4 (Nox4) is a major source of oxidative stress in the failing heart
Kuroda, J., Ago, T., Matsushima, S., Zhai, P., Schneider, M. D., & Sadoshima, J. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1002178107 · Cited by 772
Superoxide flashes in single mitochondria
Wang, W., Fang, H., Groom, L., Cheng, A., Zhang, W., Liu, J., Wang, X., Li, K., Han, P., Zheng, M., et al. (2008) · Cell · doi:10.1016/j.cell.2008.06.017 · Cited by 715
NADPH Oxidases in Cardiovascular Health and Disease
Cave, A. C., Brewer, A. C., Narayanapanicker, A., Ray, R., Grieve, D. J., Walker, S., & Shah, A. M. (2006) · Antioxidants & Redox Signaling · doi:10.1089/ars.2006.8.691 · Cited by 630
Self-citation
Cited by
Mitochondrial Reactive Oxygen Species (ROS) and ROS-Induced ROS Release
Zorov, D. B., Juhaszova, M., & Sollott, S. J. (2014) · Physiological Reviews · doi:10.1152/physrev.00026.2013 · Cited by 5,383
Mitochondrial dysfunction and oxidative stress in heart disease
Peoples, J. N., Saraf, A., Ghazal, N., Pham, T. T., & Kwong, J. Q. (2019) · Experimental & Molecular Medicine · doi:10.1038/s12276-019-0355-7 · Cited by 950
Münzel, T., Gori, T., Keaney, J. F., Maack, C., & Daiber, A. (2015) · European Heart Journal · doi:10.1093/eurheartj/ehv305 · Cited by 394
New Insights on NOX Enzymes in the Central Nervous System
Nayernia, Z., Jaquet, V., & Krause, K.-H. (2014) · Antioxidants & Redox Signaling · doi:10.1089/ars.2013.5703 · Cited by 279
Mitochondrial and cellular mechanisms for managing lipid excess
Aon, M. A., Bhatt, N., & Cortassa, S. C. (2014) · Frontiers in Physiology · doi:10.3389/fphys.2014.00282 · Cited by 253
“Keeping a proper cellular/mitochondrial RE is vital for optimal excitation-contraction (EC) coupling as well as energy supply in the heart (Burgoyne et al., 2012; Christians and Benjamin, 2012; Nickel et al., 2013, 2014).”
BackgroundInfluentialRedox interplay between mitochondria and peroxisomes
Lismont, C., Nordgren, M., Van Veldhoven, P. P., & Fransen, M. (2015) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2015.00035 · Cited by 214
Vascularized cardiac spheroids as novel 3D in vitro models to study cardiac fibrosis
Figtree, G. A., Bubb, K. J., Tang, O., Kizana, E., & Gentile, C. (2017) · Cells Tissues Organs · doi:10.1159/000477436 · Cited by 79
Mitochondrial health, the epigenome and healthspan
Aon, M. A., Cortassa, S., Juhaszova, M., & Sollott, S. J. (2016) · Clinical Science · doi:10.1042/cs20160002 · Cited by 66
Nrf2-Mediated Dichotomy in the Vascular System: Mechanistic and Therapeutic Perspective
Wu, W., Hendrix, A., Nair, S., & Cui, T. (2022) · Cells · doi:10.3390/cells11193042 · Cited by 20
Molecular Perspectives of Mitochondrial Adaptations and Their Role in Cardiac Proteostasis
Alam, S., Abdullah, C. S., Aishwarya, R., Morshed, M., & Bhuiyan, M. S. (2020) · Frontiers in Physiology · doi:10.3389/fphys.2020.01054 · Cited by 12
Metadata
- Authors
- Burgoyne, J. R., Mongue-Din, H., Eaton, P., & Shah, A. M.
- Venue
- Circulation Research
- Published
- 2012-09-28
- Volume
- 111
- Issue
- 8
- Pages
- 1091-1106
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2133203435
- Cited by
- 482
- References
- 20
- FWCI
- 13.36
- Type
- journal article
- Language
- en
- Open access
- closed
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
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.
