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Objective@#To investigate the level and trend of cardiovascular disease mortality in China from 2002 to 2016.@*Methods@#Using data of China Health Statistics Yearbook (2003-2012) and China′s Health and Family Planning Statistical Yearbook (2013-2017),we calculated the age-standardized mortality rates (ASMR) in China. Joinpoint regression model was employed to estimate the annual percent change (APC) and average annual percent change (AAPC) of cardiovascular disease ASMR.@*Results@#(1)The ASMR of cardiovascular disease were 225.65/100 thousands, 242.74/100 thousands, 214.63/100 thousands, 240.97/100 thousands, 195.24/100 thousands, 201.50/100 thousands, 208.83/100 thousands, 248.44/100 thousands, 261.38/100 thousands, 231.98/100 thousands, 210.25/100 thousands, 237.80/100 thousands, 235.21/100 thousands, 237.58/100 thousands,and 237.25/100 thousands from 2002 to 2016, and there was no significant difference in ASMR of cardiovascular disease (AAPC=0.2%, P>0.05) . The ASMR of chronic rheumatic heart disease decreased significantly (AAPC=-4.5%,P<0.05). There were no significant differences in ASMR of cerebrovascular disease, hypertensive heart disease, and ischemic heart disease (AAPC=0, P>0.05; AAPC=2.0%, P>0.05; AAPC=4.3%, P>0.05, respectively). (2) There were no significant differences in ASMR of cardiovascular disease from 2002 to 2016 in city and country (AAPC=-0.7%, P>0.05; AAPC=0.8%, P>0.05, respectively). The ASMR of chronic rheumatic heart disease decreased significantly in city and rural area (AAPC=-4.4%, P<0.05; AAPC=-4.6%, P<0.05, respectively). (3) There were no significant differences in ASMR of cardiovascular disease from 2002 to 2016 in male and female (AAPC=-0.3%,P>0.05; AAPC=-0.2%,P>0.05,respectively). The ASMR of chronic rheumatic heart disease decreased significantly in female (AAPC=-4.2%, P<0.05). The ASMR of ischemic heart disease increased significantly in male and female (AAPC=4.7%,P<0.05; AAPC=5.2%,P<0.05,respectively). (4) The ASMR of cardiovascular disease showed a significant upward trend in residents aged 15 to 34 from 2002 to 2016 (AAPC=3.1, P<0.05). There were no significant differences in ASMR of cardiovascular disease in residents aged 35 to 64 and ≥65 (AAPC=-0.1%, P>0.05; AAPC=-0.2%, P>0.05, respectively).@*Conclusion@#The ASMR of cardiovascular disease in China remains stable during 2002 to 2016, and the ASMR of cardiovascular disease shows upward trend among young people.
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Carboxyl terminus of the HSP70-interacting protein (CHIP) is a co-chaperone of HSPs as well as an E3 ubiquitin ligase, and it is the connexin between heat shock proteins and ubiquitin-proteasome system. Recent research discovered that CHIP also possesses an intrinsic chaperone activity that enables it to recognize and bind nonnative proteins independently. CHIP regulates the HSPs expression and activity, and facilitates the client proteins ubiquitination and subsequent proteasome-dependent degradation. CHIP also inhibits apoptosis through MAPKs signaling pathways, and affects eNOS specific activity by means of the effects on Akt. Moreover, CHIP plays an important role in mitochondrial oxidative stress protection. With these above points, this paper reviews the function of CHIP in myocardial ischemia/reperfusion injury.
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Objective To study the influence on heat shock protein 27 (Hsp27) and tumor necrosis factor ? (TNF-?) by inhibiting ubiquitin proteasome system in cardiac ischemia-reperfusion (I/R) rats. Methods Left anterior descending (LAD) coronary artery was ligated for 30 min and then released for 6 h in adult Sprague-Dawley rats. Five minutes before reperfusion, MG-132 (N-benzoyloxycarbonyl (Z)-Leu-Leuleucinal) at dose of 0.75 mg/kg was given by vein injection in I/R+T group, but I/R group, I group and sham group were given the same volume of sterile saline. The changes of myocardial infarct size, cardiac protein and mRNA levels of Hsp27 and TNF-? were measured. Results Compared with I/R group, the myocardial infarct size was significantly reduced (P
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Degradation of most proteins in eukaryotic cells is through the ubiquition-proteasome system(UPS).Recently,it demonstrated that UPS regulates cell apoptosis and cardiac hypertrophy.The differences of UPS regulation lie in E3 ligases,which specifically recognize targets and direct the ubiquitination process.Recent evidence suggests that atrogin-1/muscle atrophy F-box(Mafbx) and muscle RING finger 1(MuRF1) may be critical mediators of the heart and muscle atrophy and hypertrophy.This review summarizes the possible relationship between UPS and cardiac dysfunction after myocardial infarction in order to inhibit cardiac dysfunction after myocardial infarction.
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Objective To explore the influence of proteasome inhibitor, MG-132 (N-benz0y1oxycarbonyl(Z)-Leu-Leuleucina1) on the expressions of carboxyl terminus of the Hsc70-interacting protein (CHIP) and heat shock protein 70 (HSP70) in ischemia reperfusion (I/R) rats and investigate the underlying mechanism of myocardial protection by the inhibitor. Methods Totally 54 adult SD rats were randomly divided into 3 groups, sham group (n=6), I/R group (n=24) and treatment group (I/R+T, n=24). The later 2 groups were further equally divided into 3 subgroups according different time of reperfusion. Left anterior descending (LAD) coronary artery was ligated for 30 min and then released for 2 h or 24 h or 7 d in different subgroups. Five minutes before reperfusion, MG-132 at dose of 0.75 mg/kg was given intravenously in I/R+T group,but I/R group and sham group were given the same volume of normal saline. The levels of CHIP and HSP70 at mRNA and protein level were detected by real-time PCR and Western blotting respectively. The correlation between CHIP and HSP70 expression was analyzed. Results Compared with I/R groups, the mRNA levels of CHIP and HSP70 were significantly increased in I/R+T groups (P
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Objective: To investigate the effect of proteasome inhibitor MG-132 on myocardial infarction size and biochemical marker levels in rat myocardium after reperfusion injury.Methods: Adult Sprague-Dawley rats were randomly divided into 4 groups: left anterior descending(LAD) coronary artery ligation for 30 minutes without treatment(I30min),LAD ligation for 30 minutes with subsequent 6 hours reperfusion without treatment(I30min/R6h),LAD ligation for 30 minutes with subsequent 6 hours reperfusion with treatment(I30min/R6h+I30min/R6h) and Sham(Sham30min).After LAD was ligated for 25 min,at 5 min before reperfusion,MG-132(0.75mg/kg)or sterile saline was given to all the treatment group/sham rats,the myocardial infarct size,levels of serum creatine kinases(CK),CK muscle-brain fraction(CK-MB),and troponin I(TnI),were measured.Results: Compared with Sham group,the myocardial infarct size and the ratio of the volume of myocardial infarct over the total volume of left ventricular wall,as well as the levels of serum CK,CK-MB,TnI were significantly increased in I30mingroup(P
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Objective To investigate the influence of proteasome inhibitor MG-132 on inflammatory factors in rat model of myocardial ischemia/reperfusion. Methods Adult Sprague-Dawley rats were divided into 4 groups. I/R group: left anterior descending (LAD) coronary artery was ligated for 30 min, and then reperfused for 0, 1, 2, 6, 24 h; I/R+T group: MG-132 was used for treatment, and other procedures as I/R group; Sham operation group; Sham operation+T group. At 5 min before reperfusion, MG-132 (0.75 mg/kg) was given intravenously in I/R+T group and Sham operation+T group, and normal saline for I/R group and sham operation group. The changes of myocardial ultrastructure were checked, and the protein and mRNA levels of NF-?Bp65 and TNF-?, the number of PMN, the activity of MPO and survival of each group were detected. Results As compared with Sham operation group and Sham operation+T group, the protein and mRNA levels of NF-?Bp65 and TNF-?, the number of polymorphonuclear leucocytes (PMN) and the activity of myeloperoxidase (MPO) were significantly increased in I/R group (P