Absence of Inducible Nitric Oxide Synthase Reduces Myocardial Damage During Ischemia Reperfusion in Streptozotocin-Induced Hyperglycemic Mice
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We investigated the role of inducible nitric oxide synthase (iNOS) on ischemic myocardial damage and angiogenic process in genetically deficient iNOS (iNOS−/−) mice and wild-type littermates (iNOS+/+), with and without streptozotocin-induced (70 mg/kg intravenously) diabetes. After ischemia (25 min) and reperfusion (120 min), both iNOS+/+ and iNOS−/− diabetic mice (blood glucose 22 mmol/l) had myocardial infarct size greater than their respective nondiabetic littermates (P < 0.01). Myocardial infarct size (P < 0.05), apoptotic index (P < 0.005), and tissue levels of tumor necrosis factor (P < 0.01), interleukin-6 (P < 0.01), and interleukin-18 (P < 0.01) were higher in nondiabetic iNOS−/− mice compared with nondiabetic iNOS+/+ mice. As compared with diabetic iNOS−/− mice, diabetic iNOS+/+ mice showed a greater infarct size (P < 0.01) associated with the highest tissue levels of nitrotyrosine and proinflammatory cytokines, as well as apoptosis. The beneficial role of iNOS in modulating defensive responses against ischemia/reperfusion injury seems to be abolished in diabetic mice.
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Expression of NOX5 in VSMCs and in macrophages and monocytes can contribute to the development of atherosclerotic lesions.
“Expression of NOX5 in VSMCs and in macrophages and monocytes can contribute to the development of atherosclerotic lesions (622, 623).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [623]
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- Authors
- Marfella, R., Di Filippo, C., Esposito, K., Nappo, F., Piegari, E., Cuzzocrea, S., Berrino, L., Rossi, F., Giugliano, D., & D’Amico, M.
- Affiliations
- University of Campania "Luigi Vanvitelli" (IT)
- “Centro di Eccellenza Cardiovascolare,” Second University of Naples, Naples, Italy
- University of Messina (IT)
- ORCID
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2004-02-01
- Volume
- 53
- Issue
- 2
- Pages
- 454-462
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2146079216
- Cited by
- 92
- References
- 35
- Citations by year
- 2025: 1 · 2024: 1 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 3 · 2019: 2 · 2018: 2 · 2017: 3 · 2016: 1 · 2015: 8 · 2014: 7 · 2013: 5 · 2012: 8
- FWCI
- 6.03
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Archivio Istituzionale della Ricerca - Università degli Studi della Campania "Luigi Vanvitelli" (submittedVersion)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- inducible nitric oxide synthase, myocardial ischemia-reperfusion injury, streptozotocin-induced diabetes, hyperglycemia, myocardial infarct size, apoptosis, nitrotyrosine, inflammatory cytokines, TNF-α, interleukin-6, IL-18, angiogenesis, iNOS knockout mice
- MeSH terms
- Animals, Blood Glucose, Blood Pressure, Diabetes Mellitus, Experimental, Hyperglycemia, Insulin, Interleukins, Myocardial Infarction, Myocardium, Reference Values, RNA, Streptozocin, Tyrosine, Myocardial Reperfusion Injury, Mice, Knockout, Nitric Oxide Synthase, Mice, Nitric Oxide Synthase Type II
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