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A number of studies have suggested the benefits of pet ownership to human health, including cardiovascular disease (CVD). However, there are few findings regarding pet ownership and coronary artery disease (CAD). The objective of this study is to investigate the association between pet ownership and CAD in a Chinese population. From October 2015 to May 2016, a survey consisting of 561 consecutive patients was done in Nanjing, China. Based on the results of coronary arteriography for the first time, participants were divided into 2 groups (non-CAD and CAD groups). Pet ownership information was collected by using a questionnaire. After multivariate adjustments, pet ownership was associated with a decreased CAD risk (odds ratios [OR]: 0.504, 95% confidence intervals [CIs]: 0.310–0.819). There was a reduced CAD risk among dog owners (OR: 0.420, 95% CI: 0.242–0.728) when compared with the cat group (OR: 0.738, 95% CI: 0.240–2.266) and the cat and dog group (OR: 1.052, 95% CI: 0.330–3.355). With the increase of pet ownership duration, there was a decreased tendency of CAD risk, including years of keeping pets (P for trend = 0.008) and time of playing with pets per day (P for trend = 0.001). In addition, similar dose–response relationship was observed for starting age of keeping pets (P for trend = 0.002). Pet ownership, especially dog ownership, can be a protective factor for CAD in Chinese patients.

Background: In mammals, regenerative therapy after myocardial infarction is hampered by the limited regenerative capacity of adult heart, whereas a transient regenerative capacity is maintained in the neonatal heart. Systemic phosphorylation signaling analysis on ischemic neonatal myocardium might be helpful to identify key pathways involved in heart regeneration. Our aim was to define the kinase-substrate network in ischemic neonatal myocardium and to identify key pathways involved in heart regeneration after ischemic insult. Methods: Quantitative phosphoproteomics profiling was performed on infarct border zone of neonatal myocardium, and kinase-substrate network analysis revealed 11 kinases with enriched substrates and upregulated phosphorylation levels, including checkpoint kinase 1 (CHK1) kinase. The effect of CHK1 on cardiac regeneration was tested on Institute of Cancer Research CD1 neonatal and adult mice that underwent apical resection or myocardial infarction. Results: In vitro, CHK1 overexpression promoted whereas CHK1 knockdown blunted cardiomyocyte proliferation. In vivo, inhibition of CHK1 hindered myocardial regeneration on resection border zone in neonatal mice. In adult myocardial infarction mice, CHK1 overexpression on infarct border zone upregulated mammalian target of rapamycin C1/ribosomal protein S6 kinase b-1 pathway, promoted cardiomyocyte proliferation, and improved cardiac function. Inhibiting mammalian target of rapamycin activity by rapamycin blunted the neonatal cardiomyocyte proliferation induced by CHK1 overexpression in vitro. Conclusions: Our study indicates that phosphoproteome of neonatal regenerative myocardium could help identify important signaling pathways involved in myocardial regeneration. CHK1 is found to be a key signaling responsible for neonatal regeneration. Myocardial overexpression of CHK1 could improve cardiac regeneration in adult hearts by activating the mammalian target of rapamycin C1/ribosomal protein S6 kinase b-1 pathway. Thus, CHK1 might serve as a potential novel target in myocardial repair after myocardial infarction.