This open access paper is an example of one of the less well known connections between processes of aging. Loss of efficiency of the cellular maintenance processes of autophagy is a characteristic of cells in old tissues.
Here, researchers note that this dysfunction in the hematopoietic cells responsible for creating blood and immune cells also results in structure changes in bone marrow that contribute to the development of osteoporosis, the loss of bone mass and strength that occurs with age. Just because such connections are obscure doesn't mean that they are unimportant.
Osteoporosis is the outcome of an imbalance between osteoblasts that create bone and osteoclasts that break down bone tissue. Both cell populations are constantly active throughout life; bone is a dynamically remodeled tissue. With age a number of processes lead to greater osteoclast activity – easy enough to point out, but difficult to pick apart the causes and decide on a point of intervention. Cellular senescence is a contributing factor, of course, as it contributes to near all age-related conditions. Here, reduced autophagy is proposed to interfere in maintenance of the osteoblast population.
There are a few types of autophagy, involving different ways of identifying and moving unwanted proteins and structures to be engulfed by a lysosome. A lysosome is a membrane-wrapped package of enzymes that can break down most of the molecules a cell will encounter. Exactly why autophagy declines with age is an interesting question.
A great many papers cover what is known of proximate causes, changes in expression of protein machinery that regulates or is needed by different parts of the process, all of which seem to fail in their own way, as well as the accumulation of persistent metabolic waste in lysosomes, molecules that cannot be broken down by our biochemistry as it stands. The latter is fairly straightforward, but the changes in regulation and expression of proteins are ever a challenge to chase back to their underlying cause.
Source: Fight Aging!