Table 1.
RAGE Ligands | RAGE Binding Domain | Clinical Significance | Ref. |
---|---|---|---|
Endogenous RAGE Ligands | |||
AGEs | V | Diabetes, chronic inflammation and cancer | [28] |
S100/calgranulins | V or VC1 or V2 | Inflammatory response and cancer differentiation and progression | [64] |
HMGB1 | VC1C2 | Cancer development and metastasis and drug resistance | [65] |
β-sheet fibrils | V | Neuronal disease: Alzheimer’s disease | [66] |
Mac1 | RAGE-mediated leukocyte recruitment | [45] | |
Quinolinic acids | VC1 | Neuronal disease: Huntington’s disease | [67] |
LPA | V | Cell proliferation and migration in C6 glioma and smooth muscle cells | [68] |
PS | Rac1 activation in alveolar macrophages | [69] | |
C1q | Recruitment of leukocytes and phagocytosis | [70] | |
mDia1 | cytoplasmic | Initiation and activation of RAGE-mediated signaling | [13] |
Exogenous RAGE Ligands | |||
RNA or DNA | VC1 | RAGE-mediated augmentation of inflammation | [8] |
RSV F protein | VC1 | Promote the survival of RSV-infected cells | [11] |
Longistatin | V | Longistatin acts as an antagonist to RAGE and suppresses inflammation | [12] |
AGEs: Advanced glycation end-products; HMGB1: High mobility group box-1 protein; LPA: Lysophosphatidic acid; PS: Phosphatidylserine; mDia1: Mammalian diaphanous 1; RSV: Respiratory syncytial virus.