Mitochondria are the power plants of the cell, responsible for generating chemical energy store molecules to power cell processes. Urolithin A is one of a number of supplements shown to improve mitochondrial function, though as for the others it isn't all that impressive when compared to the effects of regular exercise. Nonetheless, this and other approaches to modestly attenuate age-related declines in mitochondrial function are under active development. They are not solutions to the problem of mitochondrial aging, however. For that we must look to more radical approaches to therapy, such as mitochondrial transplantation, allotopic expression of mitochondrial DNA in the cell nucleus, and partial reprogramming to reset expression of genes essential to mitochondrial function.
The aging of an organism is hallmarked by systemic loss of functional tissue, resulting in increased fragility and eventual development of age-related neurodegenerative, musculoskeletal, cardiovascular, and neoplastic diseases. Growing scientific evidence points to mitochondrial dysfunction as a key contributor in the aging process and subsequent development of age-related pathologies. Under normal physiologic conditions, the body removes dysfunctional mitochondria via an autophagic process known as mitophagy. Urolithin A (UA), a metabolite produced when gut microflora digests the polyphenol compounds ellagitannin and ellagic acid, is a known inducer of mitophagy via several identified mechanisms of action.
The primary objective of this scoping review is to identify and summarize the clinical relevance of UA supplementation in the prevention of age-related pathology and diseases. A computer-assisted literature review was performed using PubMed and EMBASE for primary source research articles examining UA supplementation and aging-related pathologies. A total of 293 articles were initially identified from a database search, and 15 articles remained for inclusion in this review, based on predetermined criteria. Analysis of the 15 identified publications demonstrated that UA holds potential as a dietary intervention for slowing the progression of aging and preventing the development of age-related disease. This review also illustrates the potential role that mitochondrial health and inflammation play in the progression of age-related pathology. Identifying the clinical relevance of UA supplementation in the prevention of age-related pathology and diseases will help further the focus of research on treatments that may improve the longevity and quality of life in patients at risk for these comorbidities.