For example, an increment in the two-day average (lag1-2) level of PM<sub>2.5</sub> by one IQR (34.4 µg/m<sup>3</sup>) was associated with a 6.3% (95%CI: 3.0%-9.8%) increase in the daily count of admissions for ischemic heart disease in Hanoi and with 23.2% (95%CI: 11.1%-36.5%) for cardiac failure in Quang Ninh.
For example, an increment in the two-day average (lag1-2) level of PM<sub>2.5</sub> by one IQR (34.4 µg/m<sup>3</sup>) was associated with a 6.3% (95%CI: 3.0%-9.8%) increase in the daily count of admissions for ischemic heart disease in Hanoi and with 23.2% (95%CI: 11.1%-36.5%) for cardiac failure in Quang Ninh.
For example, an increment in the two-day average (lag1-2) level of PM<sub>2.5</sub> by one IQR (34.4 µg/m<sup>3</sup>) was associated with a 6.3% (95%CI: 3.0%-9.8%) increase in the daily count of admissions for ischemic heart disease in Hanoi and with 23.2% (95%CI: 11.1%-36.5%) for cardiac failure in Quang Ninh.
For example, an increment in the two-day average (lag1-2) level of PM<sub>2.5</sub> by one IQR (34.4 µg/m<sup>3</sup>) was associated with a 6.3% (95%CI: 3.0%-9.8%) increase in the daily count of admissions for ischemic heart disease in Hanoi and with 23.2% (95%CI: 11.1%-36.5%) for cardiac failure in Quang Ninh.
For example, an increment in the two-day average (lag1-2) level of PM<sub>2.5</sub> by one IQR (34.4 µg/m<sup>3</sup>) was associated with a 6.3% (95%CI: 3.0%-9.8%) increase in the daily count of admissions for ischemic heart disease in Hanoi and with 23.2% (95%CI: 11.1%-36.5%) for cardiac failure in Quang Ninh.
Transplantation of miR-326-5p-overexpressing EPCs improved cardiac function for AMI therapy, which can be a novel strategy for enhancing therapeutic angiogenesis in ischemic heart diseases.
Recently, we investigated the protective effects of CALB-3 on myocardial injury and its possible mechanisms of action using a rat model of myocardial ischemia.
These observations demonstrate that enhanced GGT activity contributes to cardiac damage after myocardial ischemia/reperfusion, possibly via increased oxidative stress and subsequent norepinephrine overflow.
These observations demonstrate that enhanced GGT activity contributes to cardiac damage after myocardial ischemia/reperfusion, possibly via increased oxidative stress and subsequent norepinephrine overflow.
These observations demonstrate that enhanced GGT activity contributes to cardiac damage after myocardial ischemia/reperfusion, possibly via increased oxidative stress and subsequent norepinephrine overflow.
These observations demonstrate that enhanced GGT activity contributes to cardiac damage after myocardial ischemia/reperfusion, possibly via increased oxidative stress and subsequent norepinephrine overflow.
These observations demonstrate that enhanced GGT activity contributes to cardiac damage after myocardial ischemia/reperfusion, possibly via increased oxidative stress and subsequent norepinephrine overflow.
We conclude that KLX prevents MI-induced cardiac damages and cardiac dysfunction at least partly through attenuating NLRP3 and subsequent cardiomyocyte pyroptosis, and it is worthy of more rigorous investigations for its potential for alleviating ischemic heart disease.
Here, we report an important novel crosstalk between cardiomyocytes and fibroblasts mediated by the transfer of lncRNA-enriched extracellular vesicles (EVs) in the context of cardiac ischemia. lncRNA profiling identified two hypoxia-sensitive lncRNAs: ENSMUST00000122745 was predominantly found in small EVs, whereas lncRNA Neat1 was enriched in large EVs in vitro and in vivo.
<b>Conclusion</b>: Our results suggest a critical role for circDLGAP4 and HECTD1 in endothelial cell dysfunction induced by I/R, providing novel insight into potential therapeutic targets for the treatment of myocardial ischaemia.