Complement peptide C3a receptor 1 promotes optic nerve degeneration in DBA/2J mice.
Jeffrey M HarderPete A WilliamsCatherine E BraineHongtian S YangJocelyn M ThomasNicole E FoxworthSimon W M JohnGareth R HowellPublished in: Journal of neuroinflammation (2020)
C3AR1 was identified as a damaging neuroinflammatory factor. These data help suggest complement activation causes glaucomatous neurodegeneration through multiple mechanisms, including inflammation. Microglia and infiltrating myeloid cells expressed high levels of C3ar1 and are the primary candidates to mediate its effects. C3AR1 appeared to be a major regulator of microglia reactivity and neuroinflammatory function due to its interaction with IL10 signaling and other immune related pathways. Targeting myeloid-derived cells and C3AR1 signaling with therapies is expected to add to or improve neuroprotective therapeutic strategies.
Keyphrases
- induced apoptosis
- optic nerve
- cell cycle arrest
- oxidative stress
- bone marrow
- acute myeloid leukemia
- inflammatory response
- endoplasmic reticulum stress
- neuropathic pain
- cell death
- signaling pathway
- transcription factor
- high fat diet induced
- metabolic syndrome
- machine learning
- insulin resistance
- big data
- adipose tissue
- artificial intelligence
- brain injury