Conclusion

VASCONSUELO ANDREA

Sex Steroids and Apoptosis In Skeletal Muscle: Molecular Mechanisms

Bentham

Año: 2019; p. 165 - 167

Skeletal muscle atrophy and the loss of myofibers contribute to sarcopenia, acondition associated with normal aging. Certainly, the proapoptotic signaling isincreased in muscles of old animals. Then the key mechanism involved in theskeletal muscle loss could be apoptosis. Since it is now well established, thatskeletal muscle not only generate force and movement, apoptosis of this tissuecould have a wide spectrum of effects on organism at different levels, as basalenergy metabolism, in the storage for substrates, in the keep of core temperature,in glycemia, and in the use of oxygen and energy during movement. In addition,skeletal muscle acts as endocrine organ, thus could be regulated by own and noown hormones. Consequently, the progressive loss of skeletal muscleperformance with aging is associated with functional impairments in daily lifeactivities, the loss of independence, an increased risk of developing chronicmetabolic diseases, and an overall decrease in the quality of life.Clearly, discovering points of regulation of apoptosis process in skeletal musclewill lead to the development of therapies to deal with numerous pathologies.Although we are still far from understanding the events that occur first and triggermuscle apoptosis during aging, there is wide accord on the main role played bymitochondria. Interesting, sex steroid hormones may control mitochondrialfunctions by regulation of nuclear DNA encoded mitochondrial proteins, controlof nuclear transcription factors affecting those nuclear DNA encodedmitochondrial proteins, regulation of mtDNA encoded proteins, activatingsignaling pathways through ARs or ERs, and by control mitochondrial cationfluxes regulating mitochondrial channels. These actions regulate majormitochondrial functions, such as apoptosis. In agreement, ARs and ERs wasfound in mitochondria, suggesting that both hormones could directly act on theorganelle.