Telomere Shortening and Regenerative Capacity after Acute Kidney Injury

With advances in modern medicine leading to improved health, the percentage of the population who are elderly is increasing. Associated with increasing age is a decline in renal function and loss of renal mass.1 These alterations in renal function predict increasing risk for mortality.2 The aging kidney also associates with multiple disease states, such as cardiovascular disease,3 cancer,4 and cognitive dysfunction,5 which increase susceptibility to ischemic acute kidney injury (AKI), from which the elderly are less likely to recover.6 Telomere(definition) attrition is implicated in many diseases associated with aging, including cardiovascular disease; however, an association between telomere shortening and decreased renal repair and regeneration after injury is largely unknown.7 The role of telomeres, repetitive DNA elements located at the end of chromosomes, is to prevent unwanted chromosome shortening and recombination. The length of telomeres is regulated by telomerase, which adds tandem TTAGGG repeats to the end of chromosomes to minimize shortening.8 Unfortunately, the majority of human cell types have limited telomerase activity, and, as we age, our telomeres shorten progressively with every cell division, eventually becoming critically short and resulting in senescence(definition) and apoptosis. This has serious implications for organ repair, regeneration, and recovery from injury. In this issue of JASN , Westhoff et al. …