The DOI matches its Crossref record; 94 of the 94 references it cites were found in a registry or an index.
Mitochondrial oxidative stress and dysfunction in myocardial remodelling
Abstract
Recent experimental and clinical studies have suggested that oxidative stress is enhanced in myocardial remodelling and failure. The production of oxygen radicals is increased in the failing heart, whereas normal antioxidant enzyme activities are preserved. Mitochondrial electron transport is an enzymatic source of oxygen radical generation and can be a therapeutic target against oxidant-induced damage in the failing myocardium. Chronic increases in oxygen radical production in the mitochondria can lead to a catastrophic cycle of mitochondrial DNA (mtDNA) damage as well as functional decline, further oxygen radical generation, and cellular injury. Reactive oxygen species induce myocyte hypertrophy, apoptosis, and interstitial fibrosis by activating matrix metalloproteinases. These cellular events play an important role in the development and progression of maladaptive myocardial remodelling and failure. Therefore, oxidative stress and mtDNA damage are good therapeutic targets. Overexpression of the genes for peroxiredoxin-3 (Prx-3), a mitochondrial antioxidant, or mitochondrial transcription factor A (TFAM), could ameliorate the decline in mtDNA copy number in failing hearts. Consistent with alterations in mtDNA, the decrease in mitochondrial function was also prevented. Therefore, the activation of Prx-3 or TFAM gene expression could ameliorate the pathophysiological processes seen in mitochondrial dysfunction and myocardial remodelling. Inhibition of oxidative stress and mtDNA damage could be novel and effective treatment strategies for heart failure.
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
Oxygen-Derived Free Radicals in Postischemic Tissue Injury
Epstein, F. H., & McCord, J. M. (1985) · New England Journal of Medicine · doi:10.1056/nejm198501173120305 · Cited by 5,399
(2015) · American Journal Of Pathology · doi:10.2353/ajpath · Cited by 4,908
Resveratrol improves health and survival of mice on a high-calorie diet
Baur, J. A., Pearson, K. J., Price, N. L., Jamieson, H. A., Lerin, C., Kalra, A., Prabhu, V. V., Allard, J. S., Lopez-Lluch, G., Lewis, K., et al. (2006) · Nature · doi:10.1038/nature05354 · Cited by 4,290
Wu, Z., Puigserver, P., Andersson, U., Zhang, C., Adelmant, G., Mootha, V., Troy, A., Cinti, S., Lowell, B., Scarpulla, R. C., et al. (1999) · Cell · doi:10.1016/s0092-8674(00)80611-x · Cited by 4,139
Lagouge, M., Argmann, C., Gerhart-Hines, Z., Meziane, H., Lerin, C., Daussin, F., Messadeq, N., Milne, J., Lambert, P., Elliott, P., et al. (2006) · Cell · doi:10.1016/j.cell.2006.11.013 · Cited by 4,057
Mitochondrial diseases in man and mouse
Wallace, D. C. (1999) · Science · doi:10.1126/science.283.5407.1482 · Cited by 3,060
Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells.
Griendling, K. K., Minieri, C. A., Ollerenshaw, J. D., & Alexander, R. W. (1994) · Circulation Research · doi:10.1161/01.res.74.6.1141 · Cited by 2,735
Premature ageing in mice expressing defective mitochondrial DNA polymerase
Trifunovic, A., Wredenberg, A., Falkenberg, M., Spelbrink, J. N., Rovio, A. T., Bruder, C. E., Bohlooly-Y, M., Gidlöf, S., Oldfors, A., Wibom, R., et al. (2004) · Nature · doi:10.1038/nature02517 · Cited by 2,734
Transcriptional co-activator PGC-1α drives the formation of slow-twitch muscle fibres
Lin, J., Wu, H., Tarr, P. T., Zhang, C.-Y., Wu, Z., Boss, O., Michael, L. F., Puigserver, P., Isotani, E., Olson, E. N., et al. (2002) · Nature · doi:10.1038/nature00904 · Cited by 2,546
The epidemiology of heart failure: The Framingham Study
Ho, K. K. L., Pinsky, J. L., Kannel, W. B., & Levy, D. (1993) · Journal of the American College of Cardiology · doi:10.1016/0735-1097(93)90455-a · Cited by 2,247
Cited by
Ago, T., Kuroda, J., Pain, J., Fu, C., Li, H., & Sadoshima, J. (2010) · Circulation Research · doi:10.1161/circresaha.109.213116 · Cited by 506
Figueira, T. R., Barros, M. H., Camargo, A. A., Castilho, R. F., Ferreira, J. C. B., Kowaltowski, A. J., Sluse, F. E., Souza-Pinto, N. C., & Vercesi, A. E. (2013) · Antioxidants & Redox Signaling · doi:10.1089/ars.2012.4729 · Cited by 419
Graham, D., Huynh, N. N., Hamilton, C. A., Beattie, E., Smith, R. A. J., Cochemé, H. M., Murphy, M. P., & Dominiczak, A. F. (2009) · Hypertension · doi:10.1161/hypertensionaha.109.130351 · Cited by 367
Oxidative Stress as a Mediator of Cardiovascular Disease
Elahi, M. M., Kong, Y. X., & Matata, B. M. (2009) · Oxidative Medicine and Cellular Longevity · doi:10.4161/oxim.2.5.9441 · Cited by 360
Mitochondrial adaptations to physiological vs. pathological cardiac hypertrophy
Abel, E. D., & Doenst, T. (2011) · Cardiovascular Research · doi:10.1093/cvr/cvr015 · Cited by 263
Metadata
- Authors
- Tsutsui, H., Kinugawa, S., & Matsushima, S.
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2008-10-29
- Volume
- 81
- Issue
- 3
- Pages
- 449-456
- ISSN
- 0008-6363 (ISSN-L)
- OpenAlex
- W2111542355
- Cited by
- 377
- References
- 94
- FWCI
- 10.17
- 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
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Mitochondrial oxidative stress and dysfunction in myocardial remodelling. https://app.cochat.ai/papers/10.1093/cvr/cvn280
- The paper
- Tsutsui, H., Kinugawa, S., & Matsushima, S. (2008). Mitochondrial oxidative stress and dysfunction in myocardial remodelling. Cardiovascular Research. https://doi.org/10.1093/cvr/cvn280
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.
