Vitamin D is beneficial in many ways. It helps build strong bones, heals skin, aids in calcium absorption, and boosts the immune system. And now, thanks to research from Ronald M. Evans, an HHMI investigator at the Salk Institute for Biological Studies, it may decrease liver fibrosis as well.
When the liver is damaged, so-called hepatic stellate cells spring into action and start producing connective tissue known as collagen to stop the damage and heal the injury. However, excessive wound healing caused by chronic infections or alcoholism commonly leads to fibrosis—too much accumulated collagen—and can result in cirrhosis or liver cancer. Currently, there are no drugs that effectively reverse the damage.
Evans and his colleagues noticed that stellate cells contain high levels of vitamin D receptors and wondered if these proteins played a role in liver fibrosis. When they gave mice a synthetic version of vitamin D called calcipotriol, stellate cells stayed dormant and collagen production was blocked. On the other hand, as they reported April 25, 2013, in Cell, mice lacking the vitamin D receptor gene spontaneously developed liver fibrosis.
Because the same biological mechanisms are at work in humans, these findings could lead to new treatments for patients with liver disease. Since the Food and Drug Administration has already approved calcipotriol for the treatment of psoriasis, the researchers hope to move quickly to test it in clinical trials.