By Gurmukh Singh, IANS,
Toronto : In a new study with profound implications for patients of cardiovascular diseases, diabetes and cancer – which involve scarring of the tissue or fibrosis – Canadian researchers have found how scarring occurs and how to stop it from becoming life-threatening.
The study, conducted by the University of Ontario at Waterloo near here, in collaboration with Toronto’s Mount Sinai Hospital and London’s University College, has unravelled the origin of scarring and a possible treatment for it.
Andrew Leask, who is professor at the university and led the study, said people were unaware about the prevalence of scarring diseases and the toll they exact each year.
“It’s estimated about 40 percent of all deaths and health care costs in North America are related to scarring or fibrosis,” he said.
“Cardiovascular and other diseases including diabetes, cancer, and pulmonary fibrosis all involve scarring, which affects the organs’ ability to function. Another example is scleroderma, a progressive scarring disease affecting 300,000 people in the United States and 40,000 Canadians.”
During tissue repair, the study says, specialised cells called myofibroblasts travel to the wound to generate connective tissue to cause healing. Once their job is done, these myofibroblasts disappear from the wound.
But the problem arises when they persist and continue to make connective tissue as it can become too thick, preventing the organ from functioning properly. For instance, in the case of diabetes, this scarring could cause the kidney to shut down, requiring dialysis or a transplant.
The researchers identified a protein called glycogen synthase kinase 3 that acts as a brake on myofibroblasts to terminate tissue repair after the wound has healed.
But if this protein is impaired in an individual, there will be no braking on myofibroblasts which will keep producing connective tissue even after normal tissue repair, resulting in scarring after wounding.
In their experiments on mice with scarring diseases, the researchers also found elevated levels of a protein called endothelin-1. They used a drug already on the market to block endothelin-1 and thus prevent scarring.
Leask said though the use of this drug was still to be tested on humans, this therapy could stop fibrosis from occurring without affecting normal tissue repair.
The study has been published in the current issue of Journal of Clinical Investigation.