Fig. 1

Autophagy in the context of myocardiocyte regeneration and preservation of partially impaired myocardiocytes. Induction of myocardiocyte autophagy ameliorates regeneration strategies and increases myocardiocyte longevity. The regeneration and autophagy induction mechanisms involved the activation of several common genes, transcription factors, microRNAs (all the mentioned microRNAs must be overexpressed, not necessarily simultaneously), and epigenetics that are required for both processes. Autophagy activation induces the expression of Atg proteins that probably interfere with the proliferation signaling pathway and activate it. However, it remains to be elucidated since the signaling machinery is not fully understood. The role of autophagy in maintaining myocardiocytes' mass and function is through resolving oxidative stress, stress of the endoplasmic reticulum (ER), and reducing the lactic acid and calcium paradoxes (these functions indicated by asterisks) in the basal metabolite and ischemia as well as reperfusion. Subsequently, autophagy improves the intracellular homeostasis including contractile function and regeneration capacity of the myocardiocytes. GLP-1 group of anti-diabetic medications in addition to other factors can affect autophagy. Oxidative stress and endoplasmic reticulum stress are critical to maintaining autophagy and myocardiocyte mass from apoptosis and cell death, which are necessary to maintain cardiac function. IL interleukin, GLP-1 glucagon-like peptide-1, ROS reactive oxygen species