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The DNA Damage Response is a Potential Treatable Trait For COPD, Says Sauler

August 06, 2019
by Julie Parry

The August 1, 2019 Department of Internal Medicine’s Medical Grand Rounds, “Chronic Obstructive Pulmonary Disease (COPD): Old Myths, New Mechanisms,” was presented by Maor Sauler, MD, assistant professor of medicine (pulmonary, critical care, and sleep medicine).

Sauler highlighted what a large problem COPD is in the U.S. and globally. COPD is the third leading cause of death due to chronic illness in America. Globally, one billion people smoke cigarettes, but COPD is not only caused by smoking. Sauler detailed other causes of COPD and showed various patient presentations.

He explained that the understanding of the disease has evolved. Sauler presented five myths and systematically discredited them. He challenged the audience to not look at COPD as a single disease.

Sauler asked if there was a ‘treatable trait’ when it comes to treating patients with COPD.

“A lot of work has been done to mitigate the consequences of smoking and prevent the damage, but these don’t work well for patients. Because it is a little bit too late. Our approach is different, instead of protecting cells from being damaged, why not target the response to DNA damage.”

He dove into recent research on COPD, looking at the DNA damage response, like microRNAs such as miR-24 and cells like BRCA 1. In “Macrophage migration inhibitory factor deficiency in chronic obstructive pulmonary disease,” Sauler and team studied mouse models and looked at macrophage migration inhibitory factor (MIF) levels and found that MIF-CD74 insufficiency in the development of the disease.

“We think the DNA response is one of those important mechanisms and targeting miR-24 or MIF might be a potential therapy, but more importantly, that this is a different understanding of the disease.”

To learn more about Sauler’s work and watch Medical Grand Rounds, Yale faculty can review the Grand Rounds video or review his bio.

Submitted by Julie Parry on August 06, 2019