Academic Journal
Sodium-glucose Cotransporter 2 Inhibitors and Pathological Myocardial Hypertrophy
العنوان: | Sodium-glucose Cotransporter 2 Inhibitors and Pathological Myocardial Hypertrophy |
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المؤلفون: | Gao, Zhicheng, Bao, Jiaqi, Hu, Yilan, Tu, Junjie, Ye, Lifang, Wang, Lihong |
المساهمون: | National Natural Science Foundation of China |
المصدر: | Current Drug Targets ; volume 24, issue 13, page 1009-1022 ; ISSN 1389-4501 |
بيانات النشر: | Bentham Science Publishers Ltd. |
سنة النشر: | 2023 |
الوصف: | Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a new type of oral hypoglycemic drugs that exert a hypoglycemic effect by blocking the reabsorption of glucose in the proximal renal tubules, thus promoting the excretion of glucose from urine. Their hypoglycemic effect is not dependent on insulin. Increasing data shows that SGLT2 inhibitors improve cardiovascular outcomes in patients with type 2 diabetes. Previous studies have demonstrated that SGLT2 inhibitors can reduce pathological myocardial hypertrophy with or without diabetes, but the exact mechanism remains to be elucidated. To clarify the relationship between SGLT2 inhibitors and pathological myocardial hypertrophy, with a view to providing a reference for the future treatment thereof, this study reviewed the possible mechanisms of SGLT2 inhibitors in attenuating pathological myocardial hypertrophy. We focused specifically on the mechanisms in terms of inflammation, oxidative stress, myocardial fibrosis, mitochondrial function, epicardial lipids, endothelial function, insulin resistance, cardiac hydrogen and sodium exchange, and autophagy. |
نوع الوثيقة: | article in journal/newspaper |
اللغة: | English |
DOI: | 10.2174/1389450124666230907115831 |
الاتاحة: | http://dx.doi.org/10.2174/1389450124666230907115831 https://www.eurekaselect.com/article/download?doi=10.2174/1389450124666230907115831 https://www.eurekaselect.com/220801/article |
Rights: | https://creativecommons.org/licenses/by/4.0/legalcode |
رقم الانضمام: | edsbas.58093C16 |
قاعدة البيانات: | BASE |
DOI: | 10.2174/1389450124666230907115831 |
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