We found no associations between cumulative apron-years and IHD (IRR, 1.00; 95%CI, 0.97-1.03) or cerebrovascular disease (IRR, 1.00; 0.98-1.02) when adjusted for confounders.
<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.
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.
The equilibrative nucleoside transporter-1 (ENT1, SLC29A1) is an important drug target, as transporter inhibition is a potential treatment of ischemic heart disease, stroke, and cancer.
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.
Myocyte-specific Hif2a or ErbB1 knockout mice were generated to observe the effect of Hif2a knockdown in regulating ERBB1 expression and to examine the role of ERBB1 during myocardial ischemia and reperfusion injury.
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.
Finally, 25 non-obstructive IHD patients who had no anti-platelet agents were assessed for the relationship between coronary blood flow volume (CBFV) change and platelet aggregability as P2Y12 reaction unit (PRU) by VerifyNow P2Y12 assay system.
Theoretically, the estrogen deprivation induced by aromatase inhibitors (AIs) might cause ischemic heart disease, but empiric studies have shown mixed results.
The metabolic relevance and sexual dimorphism of TAGLN2 was also outlined by genetic variants that may modulate its expression and are associated with obesity and the risk of ischemic heart disease in men.
We believe that PSC-CM transplantation represents a potentially novel treatment for ischemic heart diseases, provided that several technological and biological limitations can be overcome.
Pharmacologic conditioning using P2Y11 agonist may be beneficial after cardiac transplantation in improving myocardial ischemia/reperfusion outcomes and decreasing graft rejection lesions.
Resina draconis inhibits the endoplasmic-reticulum-induced apoptosis of myocardial cells via regulating miR-423-3p/ERK signaling pathway in a tree shrew myocardial ischemia- reperfusion model.
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.
Over-expression of JAZF1 promotes cardiac microvascular endothelial cell proliferation and angiogenesis via activation of the Akt signaling pathway in rats with myocardial ischemia-reperfusion.
Our study demonstrates a critical role of Lin28-TNFR2 axis in CSC activation and survival, providing a novel strategy to enhance stem cell-based therapy for the ischaemic heart diseases.