[26,27]. Furthermore, several studies have indicated that the release of cathepsin B after lysosomal damage can activate NLRP3 [28,29]. Lysosomal destabilization is also associated with the NLRP3 activation induced by cholesterol crystals in macrophages [30], probably involved in the inflammation promoting atherosclerosis. There are some observations that amyloid fibrils, e.g. islet amyloid polypeptides (IAPP) and Alzheimer×s amyloid-β, can trigger NLRP3 inflammasomes [28,31] and in that way stimulate inflammation and enhance pathogenesis in type 2 diabetes and Alzheimer×s disease, respectively.
