The DOI matches its Crossref record; 379 of the 379 references it cites were found in a registry or an index.
Mitochondria and Reactive Oxygen Species: Physiology and Pathophysiology
Open accessAbstract
The air that we breathe contains nearly 21% oxygen, most of which is utilized by mitochondria during respiration. While we cannot live without it, it was perceived as a bane to aerobic organisms due to the generation of reactive oxygen and nitrogen metabolites by mitochondria and other cellular compartments. However, this dogma was challenged when these species were demonstrated to modulate cellular responses through altering signaling pathways. In fact, since this discovery of a dichotomous role of reactive species in immune function and signal transduction, research in this field grew at an exponential pace and the pursuit for mechanisms involved began. Due to a significant number of review articles present on the reactive species mediated cell death, we have focused on emerging novel pathways such as autophagy, signaling and maintenance of the mitochondrial network. Despite its role in several processes, increased reactive species generation has been associated with the origin and pathogenesis of a plethora of diseases. While it is tempting to speculate that anti-oxidant therapy would protect against these disorders, growing evidence suggests that this may not be true. This further supports our belief that these reactive species play a fundamental role in maintenance of cellular and tissue homeostasis.
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
Repertoires of Autophagy in the Pathogenesis of Ocular Diseases
Li, Y.-J., Jiang, Q., Cao, G.-F., Yao, J., & Yan, B. (2015) · Cellular Physiology and Biochemistry · doi:10.1159/000373980 · Cited by 16,304
Free radicals and antioxidants in normal physiological functions and human disease
Valko, M., Leibfritz, D., Moncol, J., Cronin, M. T. D., Mazur, M., & Telser, J. (2007) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2006.07.001 · Cited by 14,269
Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor
Palmer, R. M. J., Ferrige, A. G., & Moncada, S. (1987) · Nature · doi:10.1038/327524a0 · Cited by 10,704 · cited 1×
“Prize in 1998 [175–177].”
How mitochondria produce reactive oxygen species
Murphy, M. P. (2009) · Biochemical Journal · doi:10.1042/bj20081386 · Cited by 8,207
Autophagy fights disease through cellular self-digestion
Mizushima, N., Levine, B., Cuervo, A. M., & Klionsky, D. J. (2008) · Nature · doi:10.1038/nature06639 · Cited by 6,452
Oxygen toxicity, oxygen radicals, transition metals and disease
Halliwell, B., & Gutteridge, J. M. C. (1984) · Biochemical Journal · doi:10.1042/bj2190001 · Cited by 5,330
NF-κB AND REL PROTEINS: Evolutionarily Conserved Mediators of Immune Responses
Ghosh, S., May, M. J., & Kopp, E. B. (1998) · Annual Review of Immunology · doi:10.1146/annurev.immunol.16.1.225 · Cited by 5,182
The Nuclear Factor NF- B Pathway in Inflammation
Lawrence, T. (2009) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a001651 · Cited by 4,898
Parkin is recruited selectively to impaired mitochondria and promotes their autophagy
Narendra, D., Tanaka, A., Suen, D.-F., & Youle, R. J. (2008) · The Journal of Cell Biology · doi:10.1083/jcb.200809125 · Cited by 4,026
Itoh, K., Chiba, T., Takahashi, S., Ishii, T., Igarashi, K., Katoh, Y., Oyake, T., Hayashi, N., Satoh, K., Hatayama, I., et al. (1997) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1997.6943 · Cited by 3,999
Cited by
The role of oxidative stress in neurodegenerative diseases
Kim, G. H., Kim, J. E., Rhie, S. J., & Yoon, S. (2015) · Experimental Neurobiology · doi:10.5607/en.2015.24.4.325 · Cited by 1,355
Endoplasmic Reticulum Stress and Oxidative Stress in Cell Fate Decision and Human Disease
Cao, S. S., & Kaufman, R. J. (2014) · Antioxidants & Redox Signaling · doi:10.1089/ars.2014.5851 · Cited by 1,363
Oxidative Stress in Cancer Cell Metabolism
Arfin, S., Jha, N. K., Jha, S. K., Kesari, K. K., Ruokolainen, J., Roychoudhury, S., Rathi, B., & Kumar, D. (2021) · Antioxidants · doi:10.3390/antiox10050642 · Cited by 665
Roles of Autophagy in Oxidative Stress
Yun, H. R., Jo, Y. H., Kim, J., Shin, Y., Kim, S. S., & Choi, T. G. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21093289 · Cited by 396
Briston, T., Roberts, M., Lewis, S., Powney, B., M. Staddon, J., Szabadkai, G., & Duchen, M. R. (2017) · Scientific Reports · doi:10.1038/s41598-017-10673-8 · Cited by 152
Metadata
- Authors
- Bolisetty, S., & Jaimes, E.
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2013-03-19
- Volume
- 14
- Issue
- 3
- Pages
- 6306-6344
- ISSN
- 1422-0067 (ISSN-L)
- OpenAlex
- W2024902320
- Cited by
- 273
- References
- 379
- FWCI
- 6.99
- Type
- journal article
- Language
- en
- Open access
- gold
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: Mitochondria and Reactive Oxygen Species: Physiology and Pathophysiology. https://app.cochat.ai/papers/10.3390/ijms14036306
- The paper
- Bolisetty, S., & Jaimes, E. (2013). Mitochondria and Reactive Oxygen Species: Physiology and Pathophysiology. International Journal of Molecular Sciences. https://doi.org/10.3390/ijms14036306
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.
