Table 1.

Mechanisms involved in RGC loss in diabetic retinopathy and A1AT possible role.

Name	Molecule	Targets or Molecules Produced	Produces	Diabetic Retinopahty	A1AT Possible Effect	References
Glutamate	Glutamate		Citotoxicity	Increased	Decrease	[26,151,152]
Neurotriphins	BDNF	TrkB	Protection	Decreased	Increase through TrkB	[27,36,37,38,39,40,153]
	NGF	TrkA/Akt	Protection	Decreased	Increase through TrkA	[42,43,45,46,47,153]
		p75 NTR	Neuronal damage	Increased
	CNTF	CNTF mRNA	Protection	Decreased		[52]
	MANF		Protection			[54]
MAPK	p38	pro-inflammatory cytokines	Inflammation	Increased	Decrease
		Apoptosis	Cell loss			[22,50,56,57,58,59,154]
		Adherent proteins expression	Inflammation
	JNK	NFkB	Inflammation	Increased	Decrease	[60,155,156,157]
	ERK	VEGF	Vascular angiogenesis	Increased	Decrease VEGF through VEGFR1, VGFR2/p38 MAPK/STAT1
			Apoptosis			[62,108,109,158,159]
			Neuronal damage
		NOS1	Apoptosis	Increased	Decrease NOS1 through PKC/ERK	[56,160]
			Hyperpermeability
	GPR91	VEGF	Vascular angiogenesis	Increased	Decrease through VEGFR1, VGFR2/p38 MAPK/STAT1
			Apoptosis			[62,158,159]
			Neuronal damage
Akt	Akt	PI3K/Akt/GSK3β	Inflammation	Increased	Decrease	[66,161,162]
		IRS-1/PI3K/Akt	Inflammation	Increased	Decrease	[70,161,162]
		GLP-1R	Protection			[69]
		Akt/mTOR	Protection	Decreased	mTOR modulation	[135,163,164]
		Notch/PI3K/Akt	Apoptosis	Increased	Decrease	[128,129,161,162]
Nrf2	Nrf2	Nrf2/HO-1	Protection	Decreased		[75]
		SOX2-OT/Nrf2/HO-1	Protection	Decreased		[76]
NFkB	NFkB	NFkB/HMGB1	Inflammation	Increased	Decrease	[81,82,83,84,85,87,88,92,165,166]
		NFkB/RAGEs
		NFkB/TLR
		NFkB/ERK
ROS	ROS	SOD	Protection	Decreased	Increase through RAGEs	[97,98,102,154,158]
		Glutation peroxidase	Protection	Decreased		[94,95]
		HO-1	Protection	Decreased	Possible modulation	[94,95]
MMP	MMP9		Inflammation	Increased	Decrease	[123,158]
			Cell loss
AGEs	AGEs		Neuronal damage	Increased		[125,126]
p53	p53		Apoptosis	Increased	Decrease	[128,129,167]