Gender-biased vessel growth

A man's male hormones may ward off heart damage by helping vessels around the heart regenerate, suggest Sieveking and colleagues. Although studies have shown that estrogen helps regenerate blood vessels, both in the uterus after menstruation and around the heart after wear and tear, little is known about whether or not men make up for a lack of the female hormone. Some researchers have theorized that this disparity accounts for why men tend to suffer worse heart attacks more often and earlier in life than women. However, Sieveking and colleagues find that this trend may be due to a drop in androgens, a collective term for male hormones, as men age. Angiogenic activities like cell migration ensued after the authors treated human cells derived from the umbilical cord of a male fetus with the androgen DHT. Meanwhile, female cells failed to respond to the androgen, unless they were supplied with extra androgen receptors. In this case, angiogenic activities increased slightly, indicating that hormone sensitivity accounts for some of the gender difference. Castrated mice produced fewer androgens and fared poorly after the researchers inflicted vessel damage intended to resemble injuries that occur during a heart attack or a stroke. And treating the castrated mice with DHT hastened their recovery. Therefore, the authors suggest that androgen replacement therapy might one day be used to treat men at risk for heart disease. The therapy currently receives attention for possibly inducing other rejuvenating benefits, such as increased energy and muscle mass. However, it's been approached with caution as androgens have been shown to assist in tumor growth in prostate cancer—perhaps by stimulating cancer-promoting angiogenesis. Androgen treatments correlated with spikes in the growth factor VEGF, and blocking VEGF interrupted androgen-induced angiogenesis. However, androgens may also modulate angiogenesis by mobilizing progenitor cells known to be critical for vessel repair; the authors found that castrated mice had fewer progenitor cells in circulation after injury than those with their organs intact. Mutations underlying a rare disorder in which children rapidly age disrupt mitochondrial DNA repair, show Kamenisch and colleagues. Faulty repair leads to an accumulation of mutations in mitochondrial DNA, a molecular hallmark of growing old. Recent studies have connected the excess of mitochondrial gene mutations to signs of aging, including hair loss, bone loss, and the loss of subcutaneous fat. The early aging disorder, Cockayne syndrome (CS), is also marked by fat loss, along with sensitivity to …