Skeletal phenotypes and molecular mechanisms in aging mice

Abstract

Aging is an inevitable physiological process. With aging, bone often undergoes age-related bone loss, and then a series of bone-related diseases that seriously threaten the health of the human body can occur. The use of humans as the research object of studies of skeletal disease caused by aging faces many problems, such as long study duration, inconvenient sampling, significant influence by regional factors, and high investment. Mice are the first choice for studying the effects of aging on the skeletal system due to the similar structure and function of their motor system to that of humans, simple control, easy access, low cost, and short generation time. Therefore, this review summarizes the characteristics, limitations, scope of application, the bone phenotypes and the treatment methods of naturally aging mice and premature aging mouse models (including SAMP6 mice, Polg mutant mice, Lmna mice, Sirt6 mice, Zmpste24 mice, Tfam mice, Ercc1 mice, Werner mice and KL/KL-deficient mice). The molecular mechanisms of these aging mouse models, including the cellular DNA damage response, senescence-related secretory phenotype, telomere shortening, oxidative stress, bone marrow stem cell abnormalities and mitochondrial dysfunction, are summarized. We hope that this review will contribute to the understanding of the pathogenesis of aging related bone diseases.