Teresa Escalante

TL;DR: It is proposed that SVMP-induced hemorrhage occurs in vivo by a 'two-step' mechanism, whereby SVMPs degrade basement membrane and adhesion proteins, thus weakening the capillary wall and perturbing the interactions between endothelial cells and the basement membrane.

TL;DR: Evidence gathered support a two-step model for the pathogenesis of SVMP-induced hemorrhage: initially, hemorrhagic SVMPs bind to and hydrolyze components of the BM and associated extracellular matrix proteins that play a key role in the mechanical stability of BM.

TL;DR: The search for novel toxin inhibitors represents a potential avenue for improving the treatment of this serious aspect of snakebite envenomation, as muscle tissue regeneration after venom-induced pathological effects is often impaired, thus resulting in permanent tissue loss and dysfunction.

TL;DR: Experimental evidence suggests that degradation of type IV collagen, and perhaps also perlecan, is the key event in the onset of microvessel damage, and it is necessary to study this phenomenon from a holistic, systemic perspective in which the action of other venom components is also taken into consideration.

TL;DR: Cardiovascular disturbances leading to shock are due to the combined effects of hemorrhagic toxins, other venom components that increase vascular permeability, the action of hypotensive agents in the venom and of endogenous mediators, and the potential cardiotoxic effect of some toxins.