Potential of lipoproteins as biomarkers in acute myocardial infarction

Abstract

Acute myocardial infarction (AMI), commonly known as heart attack, is a medical emergency that is potentially fatal if not promptly and pro- perly managed. The early diagnosis of AMI is critically important for the timely institution of pharmacotherapy to prevent myocardial damage and preserve cardiac function. Ischemic insults during AMI cause myocardial tissue damage, releasing the cardiac muscle protein troponin T into the blood stream. Therefore, serum troponin T levels are used as a sensitive and specific indicator of myocardial injury for diagnosing AMI. However, there remains a requirement for developing technologies for more accurate biomarkers or signatures for AMI diagnosis or prognosis. Previous studies have implicated impaired lipid metabolism as a causative factor in AMI development. Lipoproteins are important constituents of lipid metabolism; their levels in the blood stream are a convenient biomarker tool for monitoring lipid metabolism. This review summarizes recent findings (data of studies from 2001 to 2016) regarding the biomarker potentials of various lipoproteins, including low-density lipoprotein, oxidized low-density lipoprotein, high-density lipoprotein, lipoprotein-a, and remnant lipoprotein, for the risk stratification of AMI.

MiR-223-3p affects myocardial inflammation and apoptosis following myocardial infarction via targeting FBXW7

“…After releasing their contents, necrotic cells activate the autoimmune system, resulting in a severe inflammatory response (12,13). Among the cytokines involved, the TNF, interleukin, and transforming growth factor families will further affect the survival of cardiomyocytes, change vascular endothelial function, and recruit inflammatory cells to the injured myocardium, so as to aggravate or improve the local injury of ischemic myocardium (14,15). The persistence of inflammation will lead to matrix degradation and cardiomyocyte apoptosis (16).…”

L-Borneol 7-O-[β-D-Apiofuranosyl-(1 → 6)]-β-D-Glucopyranoside Alleviates Myocardial Ischemia-Reperfusion Injury in Rats and Hypoxic/Reoxygenated Injured Myocardial Cells via Regulating the PI3K/AKT/mTOR Signaling Pathway

“…It has previously been demonstrated that the damage of myocardial structure induces the increased release of CK-MB, cTnT, AST, LDH, CK, and LDH-1 from myocardial tissues [ 38 , 39 ]. These enzymes as heart-specific biochemicals have proven valuable in the diagnosis of myocardial damage [ 40 , 41 ]. The current study found that the CK-MB, cTnT, AST, LDH, CK, and LDH-1 levels in serum were increased in MIRI rats, accompanied by an increase of LDH and CK-MB levels in H/R-injured H9c2 cells and that decreased under pretreatment with LBAG or Ver.…”

Lipid and metabolite correlation networks specific to clinical and biochemical covariate show differences associated with sexual dimorphism in a cohort of nonagenarians

“…The comparison of disease-associated networks shows that for both men and women the full spectrum of (measured) lipids is associated with the differences among networks, suggesting their central role in pathophysiological mechanisms and in their resolutions; lipids are not only engaged in inter-and intra-cellular signaling regulation pathways but are also able to orchestrate inflammation processes and to restore the homeostasis [96], which may explain also the strong lipid signature observed also in drug-treatment associated networks. In women risk factornetworks lipid components, in particular, VLDL, plays a major role: in post-menopausal women, VLDL is negatively associated with estrogens [97][98][99], and this is related to increased risk of cardiovascular diseases [100,101], myocardial infarction [102], and hyperlipidemia [103]: its association with diverse risk factors is worthy of mention since VLDL is actually being reconsidered as a potential biomarker [78,104,105]. The role of metabolites in explaining network differences is more nuanced, and this probably reflects the large biochemical diversity of these molecules [106].…”