High Mobility Group Box-1: A Missing Link between Diabetes and Its Complications

Table 2

HMGB-1: evidence in DN (diabetic nephropathy).

Involved signal molecule(s)	Notes	Ref.
HMGB-1,TLR4	Strong HMGB-1 staining was detected in proximal and distal tubules of DN biopsies.	[48]
HMGB-1, TLR2, TLR4, MyD88, NF-κB	HMGB-1 and TLRs were upregulated in kidneys of diabetic rats, which were associated with increased renal expression of MyD88 and MCP-1 and activation of NF-κB.	[49]
HMGB-1, TLR4	Upregulated expression of HMGB-1 and TLR4 in early diabetic kidney mice.	[50]
HMGB-1, TLR4, MyD88, SyK, NF-κB, TGF-1beta	ROS-dependent HMGB-1 expression led to Syk activation via binding to TLR4.	[11]
HMGB-1, NF-κB	HMGB-1 mediated the D-glucose-induced proinflammatory cytokines in mesangial cells.	[51]
HMGB-1, RAGE, TLR4, CTGF, TGF-beta	HMGB-1 enhanced AGE-induced expression of CTGF and TGF-beta via RAGE and TLR4-dependent signaling.	[35]
HMGB-1, NF-κB, TNF-α, IL-6	HMGB-1 was involved in high-glucose-induced vascular smooth muscle cell proliferation and migration.	[52]

DN: diabetic nephropathy; TLR: Toll-like receptor; MyD88: myeloid differentiation factor-88; NF-κB: nuclear factor-κB; SyK: spleen tyrosine kinase; TGF-beta: transforming growth factor-beta; RAGE: receptor for advanced glycation end products; CTGF: connective tissue growth factor; AGE: advanced glycation end product; Ref.: references.