Today, I’ll point out an open access commentary in which the authors survey a number of lines of research into age-related dysfunction in the liver, all of which lead back to elevated levels of cyclin-dependent kinase 4 (CDK4). Some of this work involves investigation of the mechanisms of fatty liver disease, more properly known as hepatic steatosis. This is most commonly caused by being overweight in this age of cheap calories, but, setting aside the morbidly obese, the condition nonetheless tends to emerge later rather than earlier in life. Other research programs look at more directly age-associated measures of liver function, such as senescent cell burden, changes in gene expression, and proteins and lipids in the bloodstream. Inhibition of CDK4 in late life to some degree reverses many of these declines.
Manipulation of specific proteins and genes is an intervention with widely varying expectations of ease and safety. The ideal gene and its protein product has little influence over anything other than the one disease-associated mechanism of interest. Or at the least, it only has that one relationship in the organ suffering from the disease state, even if it has other roles elsewhere
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