The DOI matches its OpenAlex record, with a small difference in title or year; 34 of the 34 references it cites were found in a registry or an index.
Pathophysiology of ischaemia-reperfusion injury
Abstract
In recent years, it has been shown that inflammation plays an important role in the pathogenesis of atherosclerosis. Activated macrophages, T lymphocytes, and mast cells are present in atherosclerotic plaques, which has led to the notion that the inflammatory response is an immune-mediated process. Complicated lesions, moreover, appear to be associated with an increase in the amount of the inflammatory response and in these patients, increased levels of acute phase proteins are present. The appreciation that atherosclerosis is an immune-mediated inflammatory disease has also led to renewed interest in the potential role of infectious agents in initiating or modulating atherosclerosis. Seroepidemiological studies have shown raised antibody titres against several micro-organisms. However, as yet, there are hardly any data available that provide a sound scientific basis for an infectious origin. Of all potential candidate organisms, Chlamydia pneumoniae appears as the one most likely involved in atherogenesis. C. pneumoniae has been retrieved from atherosclerotic tissues; the level of raised plasma titres correlates with the severity of symptomatic atherosclerotic disease; and the incidence of C. pneumoniae-responsive T cells in peripheral blood is increased in patients with coronary heart disease. It also appears that in some patients T cells generated from atherosclerotic plaques respond to C. pneumoniae. At the present state of knowledge, however, it is fair to state that the relationship between infection, intraplaque inflammation, and atherosclerosis still remains hypothetical, despite the increasing evidence that such a relationship could exist
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“The restored blood flow to the ischemic area can cause further tissue damage called reperfusion injury as the white blood cells (WBC) in the blood release free radicals and interleukins; oxygen delivery to the ischemic tissue damages plasma membrane, DNA and cellular protein; and plasma membrane injury may release more free radicals.”
From Ischemic bowel disease in 2021. (2021) · cites this paper as [25]
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“WBC can cause further ischemia if they bind to the endothelial cells of capillaries[25].”
From Ischemic bowel disease in 2021. (2021) · cites this paper as [25]
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Metadata
- Authors
- Carden, D. L., & Granger, D. N.
- Venue
- The Journal of Pathology
- Publisher
- Wiley
- Published
- 2000-02
- Volume
- 190
- Issue
- 3
- Pages
- 255-266
- OpenAlex
- W7132835804
- Cited by
- 5
- References
- 0
- Citations by year
- 2026: 1 · 2025: 1 · 2023: 2 · 2017: 1
- FWCI
- 0.00
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Pure Amsterdam UMC (submittedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Aortic Thrombus and Embolism
- Keywords
- atherosclerosis, inflammation, infection, Chlamydia pneumoniae, immune-mediated inflammation, macrophages, T cells, mast cells, acute phase proteins, atherosclerotic plaque, coronary artery disease, seroepidemiology, T cell response
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