Table 1.
No. | Name of Disease | Brief Etiology and Possible Role of MPO | Reference |
---|---|---|---|
1 | CVD and atherosclerosis | Raised level of MPO causes RBCs deformability, accumulation of cholesterol and its esters, ruptures in atherosclerotic plaque | [8,60] |
2 | Obesity | Neutrophil infiltration and activation of MPO in adipose tissue | [84,85] |
3 | Neurodegenerative diseases | Release of neurotoxic mediators by many factors spearheaded by MPO from neurons, astrocytes, microglia cells | [11] |
4 | Cancer | MPO-derived ROS/RNS react with major biomolecules causing mutagenesis, gene polymorphism, SNPs, acrolein-protein adduct formation | [86,87,88] |
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 | [89,90] |
6 | Renal diseases | MPO-initiated HOCl-modified proteins in glomerular peripheral basement membranes | [91] |
7 | Liver diseases | Neutrophil infiltration, hepatic fibrosis by activation of Kupffer cells cause production of oxidants, impaired signaling events | [92,93] |
8 | Lung injury | Activation and expression of proinflammatory cytokines and mediators by MPO | [5] |
9 | Cystic fibrosis | Bacterial infiltration, especially Pseudomonas aeruginosa and infiltrating neutrophils | [94] |
10 | Multiple sclerosis | MPO-generated ROS cause axonal damage by proteolytic enzymes and cytotoxic oxidants by activated immune cells and glia | [95] |
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 | [96] |
12 | Parkinson’s disease | Upregulation of MPO and its byproduct, 3-chlorotyrosine, in ventral midbrain | [97] |
13 | Tuberculosis | Enhanced MPO expression along with TNF-α and IL-12 activation | [98] |
14 | Asthma | Excessive MPO release from neutrophils in lower respiratory tract cells | [99] |
15 | Rheumatoid arthritis | Inflamed synovium intervened by lymphocytes and neutrophils leads to the release of proinflammatory mediators | [100,101] |
16 | Chronic sinusitis | Enhanced level of MPO and IL-8 in sinuses | [102] |
17 | Peptic ulcer | Free radicals formation initiated by MPO | [103] |
18 | Gastric ulcer | Neutrophil infiltration and the release of MPO into gastric mucosal tissue | [104] |
19 | Duodenal ulcer | MPO and other pro-inflammatory agents | [105] |
20 | Colitis | Increased activity of MPO and pro-inflammatory mediators like IL-1β and TNF-α | [106,107,108] |
21 | Pancreatitis | Increased MPO activity causes increased ROS that leads to this disease | [109] |
22 | Chronic periodontitis | Increased MPO activity in gingival crevicular fluid | [110] |
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.