Table 1. Involvement of HNE in diseases related to oxidative stress.
Pathologies | In vivo and in vitro data | References |
---|---|---|
Alzheimer's disease | HNE-modified proteins ↗, proteasome activity ↘, inflammation ↗, neurodegeneration ↗ | 28, 29 |
HNE-synaptosomal proteins conjugation, glucose transport ↘, mitochondrial ROS ↗, synaptic degeneration ↗ | 30 | |
HNE-induced ion homeostasis disturbance, Na+/K+ ATPase activity ↘, free Ca2+ ↗, cell degeneration ↗ | 31 | |
Parkinson's disease | HNE-modified proteins ↗, proteasome activity ↘, free radical generation ↗, oxidative stress ↗, dopaminergic cell death↗ | 32 |
HNE-modified proteins ↗, proteasome activity ↘, free radical generation↗ | 33 | |
Dopamine uptake ↘, Na+/K+ ATPase activity↘ | 35 | |
Cancer | HNE-guanosine adducts, G C to T.A mutations on p53 ↗, DNA repair mechanisms ↘ | 60, 61, 62 |
Low levels of HNE in tumor tissues compared with healthy tissues, ↘TGFβ1 | 46, 47, 4849 | |
High levels of HNE in cancer tissues | 50, 51, 52, 53, 54, 55 | |
Luminal HNE triggers the positive selection of preneoplastic cells in colorectal cancer | 14, 59 | |
Atherosclerosis | HNE-induced oxidative stress, IL-8 ↘, ICAM-1 ↘, cytotoxicity↗, endothelial barrier abilities ↘, apoptosis ↗ | 40 |
HNE-induced class A scavenger receptor synthesis, macrophage foam cells formation ↗, lipid cores formation ↗ | 37, 38 | |
Liver diseases | HNE-induced JNK pathway, hepatocytes cell death ↗ (NAFLD) | 43 |
HNE modification of ‘self'-proteins, autoimmune reactions ↗(ALD) | 2, 44 |
HNE, 4-hydroxy-2-nonenal; JNK, c-Jun N-terminal kinase; NAFLD, non-alcoholic fatty liver disease; ROS, reactive oxygen species; TGFβ1, transforming growth factor β
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