Mechanisms of Myocardial Damage Due to Hyperlipidemia: A Review of Recent Studies

Abstract

Myocardial injury and necrosis caused by hyperlipidemia have been investigated by several researchers. Their pathogenesis and molecular basis are different from those of the more common clinical ischemic myocardial injury. Hyperlipidemia leads to peroxide accumulation in the cardiomyocytes, causes lipid overload, decreases the antioxidant capacity of the body, and promotes the inflammatory response. Furthermore, hyperlipidemia causes changes in the structure and function of mitochondria in the cardiomyocytes, which results in their injury and necrosis. Many previous studies have shown that metabolic diseases (eg, obesity and diabetes) and chemical poisoning can lead to hyperlipidemic myocardial injury and necrosis. Moreover, it has been observed that this pathological process can be inhibited by many small molecular substances. In the clinic, myocardial damage can be prevented or reduced by lowering the levels of triglyceride and cholesterol. Myocardial damage can also be regulated via the molecular pathway of myocardial injury caused by hyperlipidemia so that the disease can be treated. The present article reviewed the recent findings reported on the mechanisms of myocardial damage due to hyperlipidemia.

Low levels and partial exposure to palmitic acid improves mitochondrial function and the oxidative status of cultured cardiomyoblasts

“…Lipid overload or consistent exposure to saturated levels of FFAs, such as palmitic acid, is a well-known mechanism that promotes the detrimental effects leading to myocardial toxicity [20] , [21] , [22] . In fact, lipid overload has been linked with impaired mitochondrial function, including altered respiratory process that potentially contributes to excessive production of toxic ROS, within various experimental models of metabolic disease [8] , [23] . The current state of knowledge indicates that impaired lipid profiles, especially hypercholesterolemia is major driver of lipid peroxidation, which is connected to the development of myocardial dysfunction within conditions of T2D [24] , [25] .…”

“…Like most cells, cardiac cells store FFAs as triacylglycerol and package them into cytoplasmic lipid droplets, while also remaining their predominant source of energy [6] . Emerging data indicates intramyocardial lipid excess can hinder the efficiency of the mitochondrial respiratory process, favouring an imbalance in redox status and further contributing to enhanced cellular damage [7] , [8] . Apparently, the use of in vitro H9c2 cardiomyoblasts has increasingly become an experimental model to provide insights into cellular mechanisms and responses at a molecular level, making them invaluable for drug screening and mechanistic studies [9] , [10] .…”