Asthma can Promote Cardiomyocyte Mitophagy in a Rat Model

Clinical observations have shown the risk of cardiovascular disease during asthmatic changes. Whether and how asthma causes heart failure is the subject of debate. Here, we aimed to investigate the possibility of cardiomyocyte mitophagy in a rat model of asthma. Twelve mature Wistar rats were randomly allocated into the Control and Asthmatic rats (n = 6). To induce asthma, ovalbumin was injected intraperitoneally on days 1 and 8 and procedure followed by nebulization from days 14 to 32. After 2 weeks, we performed the pathological examination of both lungs and heart using Hematoxylin-Eosin staining. Real-time PCR analysis was used to measure the expression of mitophagic factors, such as Optineurin, Pink1, and mitofusin 1 and 2. Typical changes like increased inter-alveolar septa thickness and interstitial pneumonia were evident in asthmatic lungs. In cardiac tissue, slight inflammatory response, and hydropic degeneration with an eosinophilic appearance were detected in the cytoplasm of cardiomyocytes. Real-time PCR analysis showed mitophagic response in pulmonary and cardiac tissues via upregulation of mitophagy-related genes like Optineurin and Pink-1 in asthmatic lungs and hearts compared to the control group (p < 0.05). Likewise, asthmatic changes increased the expression of genes associated with mitochondrial fusion in the lungs and heart. The expression of mitofusin1 and 2 was significantly increased following inflammatory response in pulmonary and cardiac tissues (p < 0.05). Our findings showed the expression of certain factors related to mitophagy during chronic asthmatic conditions. The findings open a new avenue in the understanding of cardiomyocyte injury during asthma.