MD2 Blockade to Prevent TLR4 Signaling Reverses Fibrosis in Mice

Researchers appear to have found a novel way to sabotage fibrosis, the condition in which regenerative processes run awry with age and cells begin building scar-like structures that disrupt normal tissue function. The approach involves blocking TLR4 signaling. Fibrosis is a feature of the decline of many organs; liver, lung, kidney, heart, and so forth. If it can be turned off comparatively simply, that would produce noteworthy gains for the health of older individuals, even when the underlying causes of regenerative disarray are not addressed. The question is always whether or not there is a good way to interfere without also altering other important cellular processes, of course.


An interesting broader context for this TLR4 signaling inhibition is the growing evidence that suggests senescent cells to be a significant contributing cause of fibrosis. Senescent cells secrete a great many disruptive, inflammatory signal molecules, and that changes the behavior of surrounding cells, usually for the worse when that signaling persists for a long time. It may or may not be the case that senescent cells directly cause increased TLR4 signaling, but it is worthy of note that TLR4 deficient mice exhibit a reduced level of cellular senescence than their peers. There are

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