Introduction: Due to its natural relationship with physiological health, skeletal muscle has been studied in a variety of contexts. Most commonly, it is analyzed during exercise to determine the adaptations caused by specific homeostatic imbalances. These imbalances pushed for more research in p53, a tumour suppressor known for regulating cellular stability.
Methods: This literature review will be a narrative review using primary studies to determine the role of p53 in hypertrophy, mitochondrial biogenesis, and angiogenesis of skeletal muscles during exercise.
Results: Differences in gene expression related to hypertrophy, mitochondrial biogenesis, and angiogenesis were observed during skeletal muscle adaptations dependent on p53 content and activity during and after exercise.
Discussion: p53 content level was shown to contribute to skeletal muscle atrophy immediately following exercise, while having minimal effect on mitochondrial biogenesis. Rather, p53 activity was seen to be a more likely effector of mitochondrial levels. Moreover, through indirect pathways, p53 appears to negatively correlate with increases of angiogenesis in skeletal muscle.
Conclusion: Research on p53 continues to express the importance of the protein beyond its role as a tumour suppressor. This review highlights alternative roles of p53 by analyzing its interactions in relation to exercise-induced adaptations of skeletal muscle.
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