Autophagy Dysfunction, Cellular Senescence, and Abnormal Immune-Inflammatory Responses in AMD: From Mechanisms to Therapeutic Potential

Table 1

Candidate senotherapies.

Cell/agent	Target (or targets)	Target SNC types	Refs
Immune-mediated SNC clearance
NK cells	NKG2D	IMR-90 cells, cancer cells	[48, 50]
Macrophages	oxPCCD36	SNCs in atherosclerotic plaques	[51]
Monocytes	MIF-CXCR2 axis	SNCs in atherosclerotic plaques	[49]
	CD44	HUVECs	[28]
Ipilimumab	CTLA-4, PD1	Cancer cells	[52]
Senolysis
D	p21^CIP1/WAF1, tyrosine kinases	Fat precursor cells	[54]
KKKQ	PI3K	Human endothelial cells, mouse BMSCs	[54]
D+Q	p21^CIP1/WAF1, p16^INK4A BCL-Xl, PAI-2, SASP	MEFs, IMR-90 cells	[54–56]
ABT-263	BCL-2, BCL-W, BCL-Xl	MEFs, IMR-90 cells, HUVECs	[27, 28, 53]
ABT-737	BCL-W, BCL-Xl	MEFs, IMR-90 cells, HUVECs	[27, 28, 53]
FOXO4-related-peptide	p53	IMR-90 cells	[61]
AP20187	p16^INK4A	Mouse BMSCs	[62]
SASP neutralization
Rapamycin	mTOR1	IMR-90 cells, MEFs	[28, 29, 53]
Metformin	IκB, IKKα/β	IMR-90 cells	[63]
JAK1/2 inhibitors	JAK1/2	Human primary preadipocytes, HUVECs	[65]
UBX0101	SASP factors	Chondrocytes	[27, 66]