Abstract: BACKGROUND: Caveolin-1 is widely distributed in various kinds of cells, such as endothelial cells, epithelial cells, and vascular smooth muscle cells, and plays an important role in promoting endothelial cell proliferation and angiogenesis. Therefore, it has been increasingly highlighted in ischemic diseases.
OBJECTIVE: To explore the effects of caveolin-1 on cardiac microvascularization, ventricular remodeling and mitochondrial respiratory function in rats with myocardial infarction based on angiotensin 1-7 signaling pathway. 
METHODS: Sixty male Sprague-Dawley rats were randomly divided into normal group (group A), model (group B), empty transfection (group C), Caveolin-1 transfection (group D) and triazamidine (an angiotensin converting enzyme 2 agonist; group E), and combination group (Caveolin-1+triazamidine), with 10 rats in each group. Administration in each group was given via the caudal vein, once a day, beginning at 12 hours after modeling. The left coronary artery ligation method was adopted to establish myocardial infarction models in the latter five groups. After 28 days of injection, cardiac function of rats was detected by color Doppler ultrasound, microvascular density was detected by cardiac gel ink staining, and pathological morphology of myocardial tissue was detected by hematoxylin-eosin staining. Mitochondrial respiratory function was detected by oxygen electrode method. The expression of Caveolin-1, angiotensin 1-7 signaling pathway and cardiac microvascular related indicators were detected by western blot assay. 
RESULTS AND CONCLUSION: Compared with group A, the cardiac function of rats in group B was significantly reduced (P < 0.05). Compared with group B, the cardiac function of rats in groups D-F was improved to different extents (P < 0.05). The cardiac function of rats was better in group F than groups D and E (P < 0.05). Compared with group A, rats in group B had damaged myocardial structure, irregular arrangement of myocardial cells, markedly inflammatory cell infiltration, and significantly decreased cardiac microvessel density (P < 0.05). Compared with group B, rats in groups D-F showed significantly improved myocardial pathomorphology and increased cardiac microvessel density (P < 0.05). The cardiac microvessel density in group F was higher than that in groups D and E (P < 0.05). Compared with group A, state 3 respiration level and respiratory control rate were significantly decreased in group B (P < 0.05), while state 4 respiration level was significantly increased (P < 0.05). Compared with group B, state 3 respiration level and respiratory control rate in groups D-F were increased (P < 0.05), while state 4 respiration level was decreased (P < 0.05). Compared with groups D and E, state 3 respiration level and respiratory control rate were increased in group F (P < 0.05), while state 4 respiration level was decreased (P < 0.05). Compared with group A, group B had significantly downregulated expressions of Caveolin-1, angiotensin converting enzyme 2, angiotensin 1-7, MAS receptor and platelet endothelial cell adhesion molecule-1 protein (P < 0.05). Compared with group B, the expressions of above proteins in groups D-F were significantly increased (P < 0.05); and compared with groups D and E, the expressions of above proteins in group F were significantly increased (P < 0.05). To conclude, Caveolin-1 can effectively improve cardiac microvessel density, ventricular remodeling and mitochondrial respiratory function in rats with myocardial infarction. The mechanism may be related to the targeted regulation of angiotensin 1-7 signaling pathway.

Key words: myocardial infarction, angiotensin 1-7 signaling pathway, Caveolin-1, cardiac microvessel, ventricular remodeling, mitochondrial respiratory function