Page 52 - Hormel Report 2023

Qi Tan, PhD
“Cell fate is not permanently locked. Unlocking the mechanisms of profibrotic
memory accumulation or cellular identity homeostasis will be the key to reprogram aberrant cells for overcoming the challenges
of treating fibrosis and aging related issues.”
Qi Tan
52 | THE HORMEL INSTITUTE // UNIVERSITY OF MINNESOTA Tissue Fibrosis and Regeneration
ASSISTANT PROFESSOR
Organ fibrosis results in a loss of normal tissue architecture and function and
is accompanied by a combination of
disrupted cell-cell interactions, adoption of abnormal cell fates and a scarred fibrotic matrix, which is leading a great deal of morbidity and mortality due to diseases such as idiopathic pulmonary fibrosis, liver cirrhosis and renal fibrosis. While fibrotic diseases are very common, very few treatments are available.
The research of Qi Tan, Ph.D., focuses on tissue fibrosis and regeneration with special focus
on lung fibrosis. Lung fibrosis including idiopathic pulmonary fibrosis (IPF) and other forms of pulmonary fibrosis are on the rise as the world population ages and are a major
and growing medical burden. While two FDA- approved therapeutics moderately slow disease progression, they do not fundamentally alter the course of these diseases. Epithelial dysfunction has emerged as a central component of the pathogenesis of lung fibrosis. Understanding how those cells lose their identities and remain
locked in aberrant states is critical to the development of more effective therapies for IPF and is the central motivation for Dr. Tan’s lab.
Cell Communications in Lung Homeostasis and Fibrosis.
The long -term goal of this project is to identify critical pathways through which to restore reparative or homeo-
static interactions between lung resident cell types, ultimately leading to more-effective repair of the lung after injury or chronic lung diseases such as pulmonary fibrosis. Specifically, we have found SFRP2 expression are consistently high in the lung fibroblasts/myofibroblasts of IPF lung from multiple scRNA-seq databases, as well as increased its expression at day 30 Bleomycin induced lung fibrosis from our aged mice compared with young mice study. We
aim to determine if modulation of SFRP2 in the fibroblasts can affect alveolar epithelial cells in both co-culture organoid model and knock out mice model.