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posted by martyb on Tuesday April 18 2017, @09:41AM   Printer-friendly
from the string-instrument? dept.

Researchers at the Stanford University School of Medicine have identified a pathway that, when mutated, drives fibrosis in many organs of the body.

The pathway underlies what have been considered somewhat disparate conditions, including scleroderma, idiopathic pulmonary fibrosis, liver cirrhosis, kidney fibrosis and more, the researchers found. These diseases are often incurable and life-threatening.

Importantly, the researchers were able to reverse lung fibrosis in mice by administering an antibody called anti-CD47 now being tested as an anti-cancer treatment.

"The variety of diseases caused by overproduction of fibroblasts has made finding a common root cause very challenging, in part because there has been no good animal model of these conditions," said Irving Weissman, MD, professor of pathology and of developmental biology. "Now we've shown that activating a single signaling pathway in mice causes fibrosis in nearly all tissues. Blocking the CD-47 signal, which protects cancer cells from the immune system, can also ameliorate these fibrotic diseases even in the most extreme cases."

The researchers hope their findings will lead to the development of a reliable treatment of many types of fibrotic diseases. They are also planning to investigate whether the anti-CD47 antibody could be an effective treatment for people with fibrosis.

Over the past eight years, researchers in Weissman's laboratory have shown that many human cancers evade the immune system by expressing high levels of a protein called CD47 on their surfaces. Blocking this protein with an anti-CD47 antibody restores the ability of the macrophages to gobble the cancer and has proven to be a promising treatment in animal models of the disease. Anti-CD47 antibody is currently undergoing a phase-1 clinical trial in humans with advanced solid tumors.

"Like in cancer, these fibroblasts are proliferating excessively beyond what should be their natural limit," Weissman said. "We therefore wondered whether they are also expressing the 'don't eat me' signal on their surfaces to protect them from the immune system."

When Wernig treated mice with c-Jun-induced lung fibrosis with daily injections of anti-CD47 antibody, the animals exhibited significantly better lung function, lived longer than their peers and cleared the fibrosis.


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  • (Score: 0) by Anonymous Coward on Tuesday April 18 2017, @07:09PM

    by Anonymous Coward on Tuesday April 18 2017, @07:09PM (#495971)

    Cardiac fibrosis is another example where it may be useful to use the therapy off-label (if it passes clinical trials).

    Inhibiting fibrosis may also be useful for superficial reasons such as reducing scar formation after surgery (especially plastic surgery).

    https://en.wikipedia.org/wiki/Cardiac_fibrosis [wikipedia.org]

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