While myeloperoxidase (MPO)-derived HOCl plays a crucial role in killing harmful bacteria, excessive production can lead to oxidative damage in proteins and DNA, contributing to various chronic diseases.
Elevated MPO levels are associated with conditions such as atherosclerosis, cancer, kidney disease, lung injury, multiple sclerosis, and neurodegenerative diseases like Alzheimer’s and Parkinson’s.
MPO is a key marker for these diseases because of its role in inflammation and oxidative stress.
Brief etiology and the direct/indirect involvement of MPO in different types of diseases.
|
No.
|
Name of Disease
|
Brief Etiology and Possible Role of MPO
|
| 1 |
CVD and atherosclerosis |
Raised level of MPO causes RBCs deformability, accumulation of cholesterol and its esters, ruptures in atherosclerotic plaque |
| 2 |
Obesity |
Neutrophil infiltration and activation of MPO in adipose tissue |
| 3 |
Neurodegenerative diseases |
Release of neurotoxic mediators by many factors spearheaded by MPO from neurons, astrocytes, microglia cells |
| 4 |
Cancer |
MPO-derived ROS/RNS react with major biomolecules causing mutagenesis, gene polymorphism, SNPs, acrolein-protein adduct formation |
| 5 |
Diabetes/diabetic retinopathy |
Neutrophil activation and the release of MPO in vessels and retina, upregulation of leukocyte adhesion molecules, and increased production of anti-MPO antibodies |
| 6 |
Renal diseases |
MPO-initiated HOCl-modified proteins in glomerular peripheral basement membranes |
| 7 |
Liver diseases |
Neutrophil infiltration, hepatic fibrosis by activation of Kupffer cells cause production of oxidants, impaired signaling events |
| 8 |
Lung injury |
Activation and expression of proinflammatory cytokines and mediators by MPO |
| 9 |
Cystic fibrosis |
Bacterial infiltration, especially Pseudomonas aeruginosa and infiltrating neutrophils |
| 10 |
Multiple sclerosis |
MPO-generated ROS cause axonal damage by proteolytic enzymes and cytotoxic oxidants by activated immune cells and glia |
| 11 |
Alzheimer’s disease |
Increased production of oxidants like advanced glycation end products, o,o′-dityrosine, lipid oxidation products, protein carbonyls, oxidized DNA, and 3-nitrotyrosine in neuronal tissues proposed by increased expression of MPO |
| 12 |
Parkinson’s disease |
Upregulation of MPO and its byproduct, 3-chlorotyrosine, in ventral midbrain |
| 13 |
Tuberculosis |
Enhanced MPO expression along with TNF-α and IL-12 activation |
| 14 |
Asthma |
Excessive MPO release from neutrophils in lower respiratory tract cells |
| 15 |
Rheumatoid arthritis |
Inflamed synovium intervened by lymphocytes and neutrophils leads to the release of proinflammatory mediators |
| 16 |
Chronic sinusitis |
Enhanced level of MPO and IL-8 in sinuses |
| 17 |
Peptic ulcer |
Free radicals formation initiated by MPO |
| 18 |
Gastric ulcer |
Neutrophil infiltration and the release of MPO into gastric mucosal tissue |
| 19 |
Duodenal ulcer |
MPO and other pro-inflammatory agents |
| 20 |
Colitis |
Increased activity of MPO and pro-inflammatory mediators like IL-1β and TNF-α |
| 21 |
Pancreatitis |
Increased MPO activity causes increased ROS that leads to this disease |
| 22 |
Chronic periodontitis |
Increased MPO activity in gingival crevicular fluid |
MPO: myeloperoxidase; CVD: cardiovascular disease; RBCs: red blood cells; ROS: reactive oxygen species; RNS: reactive nitrogen species; SNP: single nucleotide polymorphism; IL: interleukin; TNF-α: tumor necrosis factor-α. The descriptions of some of the diseases through the perspective of MPO are reviewed in this paper.
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Reference
Khan, Amjad A et al. “Myeloperoxidase as an Active Disease Biomarker: Recent Biochemical and Pathological Perspectives.” Medical sciences (Basel, Switzerland) vol. 6,2 33. 18 Apr. 2018, doi:10.3390/medsci6020033 This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
