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    • Although we have achieved a great deal of

    2023-04-20

    Although we have achieved a great deal of success in the development of tools to understand autophagy in health and disease, highly specific reagents for autophagy manipulation and deep knowledge of autophagy is required to advance the research in therapeutic treatment. Better disease (ischemia) animal models should be developed in order to understand the precise role of autophagy in disease progression. Also, the neuroprotective factors secreted in a23187 and peripheral organs remains to be further studied on the role of autophagy in ischemic brain injury (Li et al., 2015b, Li et al., 2014c; Tang et al., 2017; Wang et al., 2012). Finally, a joint effort from academic institutes and industry is in demand to develop new strategy to target autophagy for the identification of treatment of ischemic stroke.
    Acknowledgements
    Alcohol and alcoholic cardiomyopathy Alcoholism is one of the leading causes of non-ischemic dilated cardiomyopathy in developed countries, manifested by dilation and compromised function in one or both ventricles, as well as high cardiovascular morbidity and mortality [1,2]. Although clinical and experimental studies have confirmed potential benefit of light to moderate alcohol intake for the overall cardiovascular health [[3], [4], [5]], in particular coronary artery-related events [6,7], chronic heavy alcohol and binge drinking are known to trigger cardiac dysfunction, arrhythmias and A-V block [[8], [9], [10], [11]]. Nearly 1/3 of the alcoholics display overt cardiac anomalies featured by the unique type of non-ischemic dilated cardiomyopathy namely alcoholic cardiomyopathy [1,12], characterized by ventricular dilation, cardiac hypertrophy with reduced ventricular wall thickness, disturbed myofibrillary architecture, dampened myocardial contractility [13], interstitial fibrosis [14,15] and high prevalence of stroke and hypertension [8,16,17]. Nonetheless, these features are not unique to alcoholic cardiomyopathy and do not distinguish alcoholic myopathy from other types of dilated cardiomyopathies [1,2]. Cardiac remodeling in alcoholism is usually initiated by hypertrophy, which may process into decompensated cardiomyopathy and heart failure. Cardiac hypertrophy is common in human alcoholics with greater size and perimeter of cardiomyocytes [18]. Similar findings of cardiac remodeling have been noted in animal model of chronic alcohol intake [19,20]. Robust changes in cardiac contractile protein elements were reported in hearts from human alcoholics including up-regulated L-type Ca2+ channels [18]. Although the precise course and dosage of alcohol intake to trigger myocardial damage remain debatable, it is generally perceived that consumption of alcohol more than 90–120 g/day for 5 to 15 years may be associated with unfavorable changes in cardiac structure and function in human [12]. In addition, a number of clinical studies have revealed a close tie among alcohol intake, genetic variants in alcohol metabolizing enzymes such as aldehyde dehydrogenase (ALDH) and cardiac function [[21], [22], [23]]. Recent findings suggested that even moderate alcohol intake may exert subclinical adverse effects on systolic function, with a more pronounced response in those individuals carrying defective alcohol metabolizing genes [24]. It should be noted that many alcoholics with a history of heavy alcohol intake may display asymptomatic diastolic or systolic dysfunction (preclinical and asymptomatic) or symptomatic alcoholic cardiomyopathy (with clear signs and symptoms of heart failure) [12], complicating the clinical diagnosis of alcoholic cardiomyopathy. In addition to its direct cardiovascular sequelae, alcoholism may dramatically compromise cardiovascular function indirectly such as the worsened cardiovascular outcome in hypertensive subjects with heavy smoking [25]. These findings dictate the pertinent necessity of behavior intervention in the clinical management of alcoholic complications [25]. Practice of total alcohol abstinence is perhaps the most recommendable measure for the management of alcohol complications, including alcoholic cardiomyopathy [1,2].