Reviewing Changes to the Actin Cytoskeleton in Aging and their Possible Consequences

Near every system within the body and within cells undergoes some form of change and degeneration with advancing age. A vast amount of work could be carried out by the research community, for decades yet, in order to provide even a high level understanding of how every cellular component changes with age, as well as the relationships between them, as one form of dysfunction causes others. The paper here offers an example of this sort of investigation, discussing the actin cytoskeleton in the context of aging, a structure that allows cells to control shape and movement.

At some point, more of the scientific impulse to catalog everything has to be diverted into building effective therapies to treat aging based on what is already known. Biology must give rise to medicine, or else what is the point? Given that we have a fairly good catalog of the root causes of aging, the research community is equipped to build potentially effective therapies without further deep understanding of the effects of aging on every cellular component. Address the causes age-related dysfunction, and we can hope that the rest of the cell takes care of itself.

Recent study reported that dynamic mitochondrial behavior, including the balance between fusion, fission, and movement, may play pivotal roles in regulation of mitochondrial activity. Mitochondria are transported along the actin cytoskeleton by specific motor proteins. The mechanical properties of the cytoskeleton significantly differ between old and young cells. The cytoskeleton exhibits increased stiffness and a decreased capacity to reversibly form in old cells. The mechanical properties of the cytoskeleton are important for transfer of mechanical signals. Therefore, both mechanical properties and cell stiffness linked with the cytoskeleton may be associated with mitochondrial functional activity in aging cells. However, the role of the actin cytoskeleton in mitochondrial dysfunction related with aging is unclear.

There are several lines of evidence that a relationship exists between the actin cytoskeleton and aging. Perturbed integrity of the actin cytoskeleton is connected with loss of mitochondrial function and aging. Several scientists have attempted to elucidate how modulation of the cytoskeleton can control aging. Chemical and biological stimuli and mechanical signals from extracellular environments can regulate cellular behaviors. Biophysical signals modulate the mechanical properties of the cytoskeleton. The mechanical properties of cells regulate cellular behaviors, such as proliferation, differentiation, and apoptosis. The mechanical properties of the cytoskeleton dramatically change with aging. Artificial disturbance of the cytoskeleton induces aging phenotypes, such as slow proliferation and increased mitochondrial dysfunction. Aged cells treated with a cytoskeleton stabilizer exhibit reversal of aging phenotypes due to recovery of mitochondrial functional activities.

Taken together, these findings demonstrate that the cytoskeletal stability is a key factor for reversal of aging.


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