From basic mechanisms to clinical applications in heart protection, new players in cardiovascular diseases and cardiac theranostics: meeting report from the third international symposium on “New frontiers in cardiovascular research”

Abstract

In this meeting report, particularly addressing the topic of protection of the cardiovascular system from ischemia/reperfusion injury, highlights are presented that relate to conditioning strategies of the heart with respect to molecular mechanisms and outcome in patients’ cohorts, the influence of co-morbidities and medications, as well as the contribution of innate immune reactions in cardioprotection. Moreover, developmental or systems biology approaches bear great potential in systematically uncovering unexpected components involved in ischemia–reperfusion injury or heart regeneration. Based on the characterization of particular platelet integrins, mitochondrial redox-linked proteins, or lipid-diol compounds in cardiovascular diseases, their targeting by newly developed theranostics and technologies opens new avenues for diagnosis and therapy of myocardial infarction to improve the patients’ outcome.

Exercise-induced circulating extracellular vesicles protect against cardiac ischemia–reperfusion injury

“…Despite the great advances that have been achieved in basic and clinical research for cardiac I/R injury, it still lacks effective interventions in man [7, 8, 22, 24]. The protective effects of exercise against cardiac I/R injury have been well acknowledged [19, 31, 38, 50], which could be associated with reduced myocardial inflammation, minimized oxidative and nitric-oxidative stress, decreased cardiomyocyte apoptosis, and promoted angiogenesis.…”

The 10th Biennial Hatter Cardiovascular Institute workshop: cellular protection—evaluating new directions in the setting of myocardial infarction, ischaemic stroke, and cardio-oncology

“…Other types of cell death such as necroptosis are also involved [ 69 , 93 ]. Apoptosis is important in the brain, but its role in the reperfused heart is more controversial [ 17 , 59 , 62 , 68 ]. Although the mechanisms of cellular injury caused by ischaemia–reperfusion are very similar in the heart and brain, the brain is uniquely sensitive to damage caused by glutamate released from depolarized cells which causes glutamate excitotoxicity [ 45 , 83 ].…”

Amifostine Pretreatment Attenuates Myocardial Ischemia/Reperfusion Injury by Inhibiting Apoptosis and Oxidative Stress

“…What is more, the condition does not improve but worsen after myocardial reperfusion, causing myocardial ultrastructure, metabolism, and electrophysiological damage, known as ischemia-reperfusion injury [1–3]. …”