Hypoxia-inducible factors are stabilized and provide protection from ischemia and reperfusion injury in the setting of myocardial ischemia.In the setting of ischemia, myocyte-specific hypoxia-inducible factor 2A induces expression of amphiregulin, which is an epidermal growth factor that binds to epidermal growth factor receptor 1 (ERBB1) in the myocardium.
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.
These observations suggest that PCSK9 is inter-twined with inflammation with implications in atherosclerosis and its major consequence - myocardial ischemia.
Vildagliptin and sitagliptin are anti-diabetic drugs of the dipeptidyl peptidase-4 (DPP-4) inhibitors that have a protective role against cerebral ischemic stroke and cardiac ischemia reperfusion.
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.
These findings suggest that hypoxia-inducible factor 2A promotes transcription-independent induction of ERBB1 protein and implicates epidermal growth factor signaling in protection from myocardial ischemia and reperfusion injury.
Transient receptor potential vanilloid type 1 (TRPV1)is highly expressed in cardiac sensory neurons and has a crucial role in detecting myocardial ischemia.
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.
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.
Interaction between Endothelin-1 and Left Stellate Ganglion Activation: A Potential Mechanism of Malignant Ventricular Arrhythmia during Myocardial Ischemia.