{'fraction_non_alphanumeric': 0.02465233881163085, 'fraction_numerical': 0.010745891276864728, 'mean_word_length': 5.256916996047431, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Telomeres and mitochondrial function.

### Telomere Dysfunction Induces Metabolic and Mitochondrial Compromise Sahin et al Nature. 2011;470:359–365.

A new study provides insight into aging and age-related diseases by linking telomere dysfunction to a decline in mitochondrial number and function. 

Common observation, bolstered by a wealth of epidemiologic evidence, demonstrates that aging is accompanied by a profound increase in the incidence of cardiovascular disease. Understanding the mechanisms that underlie the aging process might, therefore, provide clues and even potential therapeutic targets for cardiovascular disease, as well as a host of other age-related pathologies. Unfortunately, even though there has been substantial progress in our understanding of the aging process, no single theory of why we age has emerged. Early studies analyzing what led to the senescence of cultured human cells focused on the telomere, the specialized region on the end of each chromosome. Each cell division is known to result in the shortening of overall telomere length. After multiple cell divisions, proliferating cells finally erode the telomere down to a critical length. At this point, the cell responds by invoking a DNA damage response not unlike what happens when DNA is damaged by exogenous radiation or chemicals. This damage response culminates in the activation of the tumor suppressor, p53. Once activated, p53 can, in turn, promote growth arrest, cell death, or perhaps most importantly for aging, cellular senescence. While our knowledge of telomere biology was …