By Kian Sani ’18
To age or not to age? That is the question. With a seemingly infinite array of anti-aging facial creams, it is now easier than ever to mask the external signs of aging. But can we truly counter aging in our organs?
Research conducted by Richard Lee and Amy Wagers at the Harvard Stem Cell Institute provides hope that the clinical reversal of senescence may not be pure fantasy for long. Using cardiac hypertrophy (CH)–the gradual thickening of the heart wall–as a model for age-related disease, Lee and Wagers engaged in a collaborative effort to determine whether the development of CH is influenced by the concentration of small molecules in the blood called circulating factors.
Like humans, mice can begin to develop CH as they age. In an attempt to reverse CH, Lee and Wagers used a novel technique known as heterochronic parabiosis–the physical joining of two organisms’ circulatory systems–to expose old mice with CH to the blood of young mice. Using this method, the researchers were able to reverse CH and restore the hearts of old mice to the physiological state of young mouse hearts. Using cutting-edge protein analysis, they discovered a circulating factor known to developmental biologists as growth development factor 11 (GDF 11).
GDF 11 is present in relatively low concentrations in old mice and in greater amounts in young mice. To confirm their hypothesis that higher concentrations of GDF 11 maintain healthy myocardial thickness, Lee and Wagers synthetically restored GDF 11 to young-mice levels in old mice and subsequently observed the reversal of CH.
The question that remains unanswered is: can we give affected individuals GDF 11 to reverse CH in humans? It turns out that the mere administration of GDF 11 without other compounds can have adverse physiological effects, so further research must be done to take GDF 11 from the bench to the bedside. In time, however, “The Curious Case of Benjamin Button” may not be so curious after all.