Chronic obstructive pulmonary disease (COPD) is a leading cause of death worldwide, but the biological mechanisms that drive the disease—especially lung damage known as emphysema—are still not fully understood.  

A new study led by Dávid Deritei, PhD, Edwin K. Silverman, MD, PhD, and Kimberly Glass, PhD, of the Channing Division of Network Medicine at Mass General Brigham, focuses on a gene called HHIP, which has long been identified as a top risk gene for COPD across multiple studies, but whose role in the disease has remained unclear. Erzsébet Ravasz Regan, PhD, of Wooster College is co-senior author. 

In this study, the researchers propose that COPD susceptibility may be driven in part by faulty wound healing in the lung that is caused by HHIP dysfunction. 

This dysfunction causes cells that normally act to heal damaged lung tissue to transform into mesenchymal cells that can’t properly restore the integrity of the tissue. Over time, this faulty repair process can contribute to emphysema, a hallmark feature of COPD. 

The team’s findings offer a mechanistic explanation for a long‑standing genetic link to COPD. These findings could also lead to new therapeutic strategies that could aim to restore proper repair signaling via the HHIP gene. 

Published in PNAS on May 26, 2026| Read the paper: “HHIP’s Dynamic Role in Epithelial Wound Healing Reveals a Potential Mechanism of COPD Susceptibility”