The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Chronic Inflammation and Oxidative Stress as a Major Cause of Age- Related Diseases and Cancer
Abstract
Chronic inflammation is a pathological condition characterized by continued active inflammation response and tissue destruction. Many of the immune cells including macrophages, neutrophils and eosinophils are involved directly or by production of inflammatory cytokine production in pathology of chronic inflammation. From literatures, it is appear that there is a general concept that chronic inflammation can be a major cause of cancers and express aging processes. Moreover, many studies suggest that chronic inflammation could have serious role in wide variety of age-related diseases including diabetes, cardiovascular and autoimmune diseases. Inflammatory process induces oxidative stress and reduces cellular antioxidant capacity. Overproduced free radicals react with cell membrane fatty acids and proteins impairing their function permanently. In addition, free radicals can lead to mutation and DNA damage that can be a predisposing factor for cancer and age-related disorders. This article reviews the antioxidant defense systems, free radicals production and their role in cancer and age related diseases and also some of the recent patent relevant to the field. Study of the role of free radicals in human diseases can help the investigators to consider the antioxidants as proper agents in preventive medicine, especially for cancer and aging processes.
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
Coussens, L. M., & Werb, Z. (2002) · Nature · doi:10.1038/nature01322 · Cited by 15,111
The biology of VEGF and its receptors
Ferrara, N., Gerber, H.-P., & LeCouter, J. (2003) · Nature Medicine · doi:10.1038/nm0603-669 · Cited by 9,591
Free radicals, metals and antioxidants in oxidative stress-induced cancer
Valko, M., Rhodes, C. J., Moncol, J., Izakovic, M., & Mazur, M. (2006) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2005.12.009 · Cited by 6,680
Metals, Toxicity and Oxidative Stress
Valko, M., Morris, H., & Cronin, M. (2005) · Current Medicinal Chemistry · doi:10.2174/0929867053764635 · Cited by 5,018
Points of control in inflammation
Nathan, C. (2002) · Nature · doi:10.1038/nature01320 · Cited by 2,738
Role of oxygen radicals in DNA damage and cancer incidence
Valko, M., Izakovic, M., Mazur, M., Rhodes, C. J., & Telser, J. (2004) · Molecular and Cellular Biochemistry · doi:10.1023/b:mcbi.0000049134.69131.89 · Cited by 1,820
Hussain, S. P., Hofseth, L. J., & Harris, C. C. (2003) · Nature Reviews Cancer · doi:10.1038/nrc1046 · Cited by 1,690 · cited 1×
“Cancer promotion can be explained by a consequence of extensive and continued free-radical related damage [74].”
BackgroundMice deficient in tumor necrosis factor-α are resistant to skin carcinogenesis
Moore, R. J., Owens, D. M., Stamp, G., Arnott, C., Burke, F., East, N., Holdsworth, H., Turner, L., Rollins, B., Pasparakis, M., et al. (1999) · Nature Medicine · doi:10.1038/10552 · Cited by 839
Role of Oxidant Species in Aging
Stadtman, E. R. (2004) · Current Medicinal Chemistry · doi:10.2174/0929867043365341 · Cited by 368 · cited 1×
“The role of protein modification in aging is illustrated by different enzymes isolated from younger animals that are catalytically more active and more heat stable than the same enzymes isolated from older animals [85].”
BackgroundIntramitochondrial signaling: interactions among mitoKATP, PKCε, ROS, and MPT
Costa, A. D. T., & Garlid, K. D. (2008) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.01189.2007 · Cited by 238
Cited by
Oxidative stress, aging, and diseases
Liguori, I., Russo, G., Curcio, F., Bulli, G., Aran, L., Della-Morte, D., Gargiulo, G., Testa, G., Cacciatore, F., Bonaduce, D., et al. (2018) · Clinical Interventions in Aging · doi:10.2147/cia.s158513 · Cited by 3,979
Nrf2 signaling pathway: pivotal roles in inflammation
Ahmed, S. M. U., Luo, L., Namani, A., Wang, X. J., & Tang, X. (2017) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2016.11.005 · Cited by 1,794
Rudrapal, M., Khairnar, S. J., Khan, J., Dukhyil, A. B., Ansari, M. A., Alomary, M. N., Alshabrmi, F. M., Palai, S., Deb, P. K., & Devi, R. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.806470 · Cited by 1,084
Small Molecule Modulators of Keap1‐ Nrf2‐ ARE Pathway as Potential Preventive and Therapeutic Agents
Magesh, S., Chen, Y., & Hu, L. (2012) · Medicinal Research Reviews · doi:10.1002/med.21257 · Cited by 760
“Recently, synthesis of novel chalcone derivatives and their SAR on ARE induction identified 2-trifluoromethyl-2′-methoxychalone (8) as a potent activator of Nrf2.”
BackgroundKaempferol and inflammation: from chemistry to medicine
Devi, K. P., Malar, D. S., Nabavi, S. F., Sureda, A., Xiao, J., Nabavi, S. M., & Daglia, M. (2015) · Pharmacological Research · doi:10.1016/j.phrs.2015.05.002 · Cited by 619
Metadata
- Authors
- Khansari, N., Shakiba, Y., & Mahmoudi, M.
- Venue
- Recent Patents on Inflammation & Allergy Drug Discovery
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2009-01-01
- Volume
- 3
- Issue
- 1
- Pages
- 73-80
- ISSN
- 1872-213X (ISSN-L)
- OpenAlex
- W2096401930
- Cited by
- 921
- References
- 10
- FWCI
- 14.39
- 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: Chronic Inflammation and Oxidative Stress as a Major Cause of Age- Related Diseases and Cancer. https://app.cochat.ai/papers/10.2174/187221309787158371
- The paper
- Khansari, N., Shakiba, Y., & Mahmoudi, M. (2009). Chronic Inflammation and Oxidative Stress as a Major Cause of Age- Related Diseases and Cancer. Recent Patents on Inflammation & Allergy Drug Discovery. https://doi.org/10.2174/187221309787158371
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.