Researchers have suggested that normal physiological processes, such as the functional integrity of muscles and bone mass, can be affected by microgravity during spaceflight. During the lifespan, bone not only develops as a structure designed specifically for mechanical tasks but also adapts for efficiency. 

Life on Earth developed under the influence of normal gravity (1g). The lack of weight-bearing forces makes microgravity an ideal physical stimulus to evaluate bone cell responses. One of the most serious problems induced by long-term weightlessness is a bone mineral loss.

In this study, they found that;

(1) Simulated microgravity and pharmacological antagonism of TRPC channels reduced cell proliferation, retarded cell cycle progression and induced cellular senescence

(2) Simulated microgravity concomitantly inhibited TRPC6 expression (while not affecting TRPC1 expression). TRPC6 may hence potentially play a role in mediating the effects on proliferation and cell cycle distribution that were observed upon simulated microgravity. 

Further studies including modulation of TRPC6 are needed to reveal the possible involvement of TRPC6 in IVD mechanotransduction.

Results from in vitro studies that entailed the use of bone cells in spaceflights showed a modification in cell attachment structures and cytoskeletal reorganization, which may be involved in bone loss. 

Exposure To Microgravity

Humans exposed to microgravity conditions experience various physiological changes, including loss of bone mass, muscle deterioration, and immunodeficiency. In vitro models can be used to extract valuable information about changes in mechanical stress to ultimately identify the different pathways of mechanotransduction in bone cells.

Bone Loss 

Despite many in vivo and in vitro studies under both real microgravity and simulated conditions, the mechanism of bone loss is still not well defined. The objective of this review is to summarize the recent research on bone cells under microgravity conditions based on advances in the field.