Varisco Research Lab

The principal function of the lung is to facilitate the absorption of oxygen and elimination of carbon dioxide. This exchange occurs in alveolus when gases cross thin alveolar and capillary membranes. Premature birth often impairs alveolar formation and lung injury can reduce the number and function of alveoli. Postnatally, a host of pathologic conditions can lead to alveolar destruction and reduced lung function. Our laboratory is focused on understanding the mechanisms which govern alveolar growth and regeneration and how alveolar and pulmonary microvascular growth are coordinated to maximize ventilation/perfusion matching.

More specifically, our laboratory is focused on how lung stretch regulates lung matrix remodeling and coordinates alveologenesis and pulmonary vascular morphogenesis. Elastin is critical for normal lung function and elastin remodeling is also important in angiogenesis in during repair of other organs and in some cancers. We have demonstrated that lung elastin remodeling is dynamically regulated in both lung development and lung regeneration, that this remodeling localizes to suspected areas of alveolar growth, and that the remodeling is associated pulmonary angiogenesis.

Stretch-regulated Remodeling of Lung Elastin by Cela1

Current Projects

How Stretch Regulates Lung Matrix Remodeling in Development and Disease 

The human lung begins as a foregut outpouching of the ventral foregut during the 4th-5th week of gestation subsequently progresses through a series of developmental stages culminating in a gas-exchanging organ with a surface area of ~750 square feet and a vasculature that matches right ventricular output to the bulk flow of atmospheric gas. While we understand many of the critical events in early lung morphogenesis, we understand less about how the lung forms these gas exchanging units (alveoli), how these pathways and processes are altered in states of impaired development (i.e. bronchopulmonary dysplasia or destruction (i.e. emphysema), and how we might halt these destructive processes and promote lung development and regeneration. Since the late prenatal and postnatal lungs exist within the cyclic stretch of the respiratory cycle, we focus on understanding how mechanosensitive and mechanotransductive inputs regulate morphogenesis of the late prenatal and postnatal lung.

Lab Projects

  • Impact of Congenital Diaphragmatic Hernia and Fetal Tracheal Occlusion on Lung Development
  • Role of Chymotrypsin-like Elastase 1 in Alveolar Development
  • Role of Chymotrypsin-like Elastase 1 in α1-antitrypsin Deficient Emphysema
  • Molecular Mechanism of Interaction between Chymotrypsin-like Elastase 1 and α1-antitrypsin
  • Alveolar Development in Adolescent Idiopathic Scoliosis and Effect of Posterior Spinal Fusion
  • Gene Expression Profiling to Identify Pediatric ARDS Endotypes

Learn more about our current projects

Contact Us

A photo of Brian Varisco.

Brian M Varisco MD
Division of Critical Care Medicine
Cincinnati Children's Hospital Medical Center

Mailing Address:
3333 Burnet Avenue
Cincinnati, OH 45229-3039

Office Phone: 513-803-2485
Fax: 513-803-3311
Email: brian.varisco@cchmc.org