Journal
CURRENT MEDICINAL CHEMISTRY
Volume 25, Issue 13, Pages 1501-1509Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/0929867324666170616105639
Keywords
Obese insulin-resistance; ischemia/reperfusion; heart; myocardial infarction; ishemic heart disease; obesity
Funding
- Thailand Research Fund [RSA5880015, RTA6080003]
- National Science and Technology Development Agency Thailand
- Chiang Mai University Center of Excellence Award
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Background: Obese insulin-resistance is one of the most important risk factor for cardiovascular diseases including ischemic heart disease (IHD). Growing evidences suggest that the susceptibility to myocardial ischemia-reperfusion (I/R) injury is increased in an obese insulin-resistance condition. Based on the currently available evidence from human and animal studies, this review mainly focuses on the influence of obese insulin-resistance on the outcome of the I/R insult to the heart. Moreover, we have discussed whether improving insulin sensitivity by pharmacological interventions could ameliorate reperfusion induced myocardial injury. Methods: The electronic database Pubmed was used as the source of selected peer-reviewed research articles published in English. Both pre-clinical studies and clinical trials were obtained using obesity, insulin resistance, ischemia-reperfusion injury and myocardial infarction as keywords. Results: Twenty-seven pre-clinical studies were obtained using obesity, insulin resistance, and cardiac ischemia-reperfusion injury as keywords, and five clinical trials were obtained using obesity, insulin resistance, and myocardial infarction as keywords. The underlying mechanisms responsible for the exacerbation of I/R injury in obese insulin resistance were the main subject of our review. Conclusion: The findings of this review suggest that the susceptibility to I/R injury is increased in an obese insulin-resistance condition. However, the underlying mechanisms responsible for the exacerbation of I/R injury in obese insulin-resistance have not been fully elucidated, but increased basal oxidative stress, the impairment of anti-oxidant capacities, insulin signaling and pro-survival signaling and increased inflammation, likely play an important role.
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