An interesting paper that uses ALA to shore up telomerase activity, loss of telomeres inhibition of P53 expression and mitochondrial dysfunction in one go. They use ALA (alpha lipoic acid) to induce PGC-1α in this case though PGC1-alpha seems to be a potential target for intervention as I understand that ALA is difficult to deliver to cells. In this case this involves the vascular system and atherosclerosis.
http://www.cell.com/cell-reports/abstract/S2211-1247(15)00825-6
Short telomeres and Mitochondrial dysfunction are increasingly implicated as being closely linked as this 2012 Dephino paper demonstrates in the aging heart:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3718635/
“On a mechanistic level, recent reports linking telomere dysfunction to metabolic and mitochondrial compromise provide a novel mechanism as to how dysfunctional telomeres can compromise cardiac function. This telomere-p53-PGC-mitochondrial axis aligns with many changes seen in aged hearts: impaired OXPHOS, decreased ATP generation, and increased ROS levels”
PGC-1α Deficiency Augments Vascular Aging and Atherosclerosis, Coinciding with Telomere Dysfunction and Shortening and DNA Damage through TERT Downregulation.
(A) The aortas from PGC-1α+/+ApoE−/− and PGC-1α−/−ApoE−/− mice (18-month-old males, standard diet, n = 5) were excised for SA-βG staining.
(B) The aortic arch from PGC-1α−/−ApoE−/− and control mice (18-month-old males, n = 5) was dissected for examination of atherosclerotic lesion formation.