Table 1.

The molecular mechanisms of HBP in various diseases.

Disease	Molecular mechanisms	Reference
Sepsis
Circulatory failure	HBP interacts with GAGs and activates the PKC and Rho-kinase pathways to increase endothelial cell permeability.	[43]
AKI	HBP activates M1 macrophages during the initial inflammation response, and suppression of HBP expression by heparin injection in septic mice results in a reduction in renal injury severity.	[67]
ALI/ARDS	HBP levels dramatically increase and exhibit significant correlation with lung wet/dry ratio and BALF total proteins. Additionally, HBP plays an important role in the alteration of lung vascular permeability in ARDS.	[73]
Bacterial skin infection	M protein induces HBP release during skin infection, and this directly and indirectly contributes to a number of profound pathophysiological effects such as endothelial hyperpermeability and neutrophil recruitment.	[11, 75]
Leptospirosis	HBP is induced by leptospires and their secreted products through a controlled degranulation mechanism that is not mediated by fibrinogen and β2 integrins.	[32]
Protozoan parasites	HBP plays a vital role in the attachment and invasion process of a variety of intracellular pathogens, and HBP even participates in the life cycle of certain parasites.	[81–86]