Does the OPN-LOX axis facilitate the formation of insoluble collagen and alter LV mechanical properties in patients with HHD and HF?
The OPN-LOX axis may play a key mechanistic role in driving myocardial fibrosis, LV stiffness, and systolic dysfunction in heart failure.
An excess of OPN is associated with increased LOX and insoluble collagen, as well as with LV stiffness and systolic dysfunction in patients with HHD and HF. In addition, OPN up-regulates LOX in human fibroblasts. It is suggested that the OPN-LOX axis might facilitate the formation of insoluble collagen (i.e. stiff and resistant to degradation) and the subsequent alteration in LV mechanical properties and function in patients with HHD and HF.
López et al. (Thu,) studied this question.
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