Introduction to MPO
Myeloperoxidase (MPO) is a peroxidase enzyme encoded by the MPO gene on chromosome 17. MPO is most expressed in neutrophils (a subtype of white blood cells) and produces hypochlorous acid for antimicrobial activity, including hypochlorous acid, whose sodium salt is a chemical in bleach. It is a lysosomal protein that is stored in nitrophilic granules of neutrophils and released into the extracellular space upon degranulation. The 150 kDa MPO protein is a cationic heterotetramer consisting of two 15 kDa light chains and two weight-variable glycosylated heavy chains bound to a restorative heme group arranged in a heterodimer.
Myeloperoxidase (MPO), also known as peroxidase, is a heme protease of heme protease of heme prosid, and is a member of the heme peroxidase superfamily.
MPO** is found in neutrophils, monocytes and macrophages. The essence of MPO is a metal tetrameric glycosylated protein with a molecular weight of 140 kDa and consists of two heavy chains and two light chains, 55 and 13, respectively5 kda。It is mainly stored in azure-loving granules of neutrophils.
MPO is a marker of neutrophil activation, and its level and activity represent the function and state of granulocytes. Under physiological conditions, MPO uses chlorine and hydrogen peroxide as substrates to catalyze the production of reactive substances such as hypochlorous acid and a variety of free radicals to fight the invasion of bacteria, fungi and other pathogenic bacteria, which is an important part of the implementation of innate immunity. When the body is in a state of inflammation and oxidative stress, it will lead to oxidative stress and oxidative tissue damage, which is involved in the occurrence of a variety of diseases, such as inflammation, tumors, neurodegenerative changes, and cardiovascular diseases.
Mainly present in neutrophils or monocytes of aniline blue granules, neutrophils degranulate and release MPO during inflammation, which can lead to instability or even rupture of coronary atherosclerotic lesions, exposing the subendothelial collagen tissue of blood vessels, followed by platelet adhesion aggregation and thrombosis, resulting in coronary artery occlusion, acute coronary syndrome (ACS) and severe myocardial irreversible ischemic damage.
MPO and the mechanism of cardiovascular disease.
MPO has been very active in the study of cardiovascular disease in recent years, and there is a direct correlation between MPO levels and the likelihood of severe symptoms in patients with chest pain or suspected coronary artery disease.
Atherosclerosis is a chronic inflammatory process that plays a key role in the occurrence, progression, and complications of atherosclerosis. During inflammation, after PMNS is activated, MPO is released into phagosomes and extracellular, and interacts with H2O2 to generate a series of reactive oxygen species with a wide range of biological effects, such as HoCl, NO2, tyrosine, etc. MPO oxidizes and modifies the lipids, apolipoproteins and antioxidants in low-LDL and high-density lipoproteins through the HOC and NO2 oxidation pathways or through the nitrification of tyrosine, resulting in the formation of lipid-filled foam cells and impaired cholesterol reverse transport function, thereby enlarging the lipid nucleus rich in cholesteryl esters and promoting the occurrence and development of plaques. As a catalytically active protein, MPO can reduce the level of the anti-inflammatory molecule nitric oxide (NO) and can produce oxidant precursors such as HoCl, tyrosyl or NO2.
MPO can be used as a risk marker for coronary artery disease.
A large number of clinical studies have shown that the change of MPO level is closely related to the incidence of myocardial infarction (AMI), and the serum MPO content in patients with acute coronary syndrome (ACS) is significantly increased, so MPO can be used as a new factor for cardiovascular adverse events in patients with acute coronary syndrome (ACS), especially in the case of low troponin levels, MPO can identify those high-risk patients who will have cardiac adverse events (MACE).
Advantages of MPO over other markers.
Myocardial injury is often an irreversible process, and it is difficult to recover necrotic myocardial cells after myocardial injury, while MPO can treat the disease before myocardial injury occurs.
Compared with other clinical markers, MPO can effectively compensate for the occurrence of cardiac adverse events in patients with troponin T always negative, and the area under the curve of MPO is significantly higher than that of troponin T, CK-MB, and C-reactive protein negative patients.
A large number of in vitro studies and pathophysiological studies have confirmed that MPO plays an important role in the initiation of cardiovascular disease and acute cardiovascular events, and the detection of MPO means that it is possible to detect and intervene in the development of coronary heart disease at an earlier stage.