Improved methodology for efficient establishment of the myocardial ischemia-reperfusion model in pigs through the median thoracic incision

To investigate the feasibility and effectiveness of establishing porcine ischemia-reperfusion models by ligating the left anterior descending(LAD)coronary artery,we first randomly divided 16 male Bama pigs into a sham group and a model group.After anesthesia,we separated the arteries and veins.Subsequently,we rapidly located the LAD coronary artery at the beginning of its first diagonal branch through a mid-chest incision.Then,we loosened and released the ligation line after five minutes of pre-occlusion.Finally,we ligated the LAD coronary artery in situ two minutes later and loosened the ligature 60 min after ischemia.Compared with the sham group,electrocardiogram showed multiple continuous lead ST-segment elevations,and ultrasound cardiogram showed significantly lower ejection fraction and left ventricular fractional shortening at one hour and seven days post-operation in the model group.Twenty-four hours after the operation,cardiac troponin T and creatine kinase-MB isoenzyme levels significantly increased in the model group,compared with the sham group.Hematoxylin and eosin staining showed the presence of many inflammatory cells infiltrating the interstitium of the myocardium in the model group but not in the sham group.Masson staining revealed a significant increase in infarct size in the ischemia/reperfusion group.All eight pigs in the model group recovered with normal sinus heart rates,and the survival rate was 100%.In conclusion,the method can provide an accurate and stable large animal model for preclinical research on ischemia/reperfusion with a high success rate and homogeneity of the myocardial infarction area.

Research progress on myocardial regeneration: what is new?

The regeneration capacity of cardiomyocytes(CMs)is retained in neonatal mouse hearts but is limited in adult mouse Myocardial infarction(MI)in adult hearts usually leads to the loss of large amounts of cardiac tissue,and then accelerates the process of cardiac remodeling and heart failure.Therefore,it is necessary to explore the potential mechanisms of CM regeneration in the neonates and develop potential therapies aimed at promoting CM regeneration and cardiac repair in adults.Currently,studies indicate that a number of mechanisms are involved in neonatal endogenous myocardial regeneration,including cell cycle regulators,transcription factors,non-coding RNA,signaling pathways,acute inflammation,hypoxia,protein kinases,and others.Understanding the mechanisms of regeneration in neonatal CMs after MI provides theoretical support for the studies related to the promotion of heart repair after MI in adult mammals.However,several difficulties in the study of CM regeneration still need to be overcome.This article reviews the potential mechanisms of endogenous CM regeneration in neonatal mouse hearts and discusses possible therapeutic targets and future research directions.

Protein kinases in cardiovascular diseases

Cardiovascular disease(CVD)remains the leading cause of death worldwide.Therefore,exploring the mechanism of CVDs and critical regulatory factors is of great significance for promoting heart repair,reversing cardiac remodeling,and reducing adverse cardiovascular events.Recently,significant progress has been made in understanding the function of protein kinases and their interactions with other regulatory proteins in myocardial biology.Protein kinases are positioned as critical regulators at the intersection of multiple signals and coordinate nearly every aspect of myocardial responses,regulating contractility,metabolism,transcription,and cellular death.Equally,reconstructing the disrupted protein kinases regulatory network will help reverse pathological progress and stimulate cardiac repair.This review summarizes recent researches concerning the function of protein kinases in CVDs,discusses their promising clinical applications,and explores potential targets for future treatments.