Vincent Auyeung, MD

Asst Professor In Residence

Medicine

Research Description:

My lab studies how cellular stress responses in the lung epithelium regulate lung epithelial plasticity and differentiation across lung diseases from asthma to pulmomary fibrosis. We have a special interest in endoplasmic reticulum stress (ER stress) and the unfolded protein response. We use a combination of mouse genetics, advanced tissue culture approaches, and novel chemical biology tools.

Our active projects include:
1. Cell and molecular biology of Regulated IRE1α-Mediated Decay (RIDD) in epithelial fate transitions
2. Fate and function of epithelial transitional states in pulmonary fibrosis
3. Regulation of goblet cell metaplasia in asthma and other muco-obstructive diseases

Primary Thematic Area:

Developmental & Stem Cell Biology

Secondary Thematic Area:

Tissue / Organ Biology & Endocrinology

Research Summary:

Stress signaling and epithelial plasticity in lung disease

Publications:

Vincent Auyeung, MD

Impaired Myofibroblast Proliferation is a Central Feature of Pathologic Post-Natal Alveolar Simplification.

BCL-2 Modulates IRE1α Activation to Attenuate ER Stress and Pulmonary Fibrosis.

IRE1α drives lung epithelial progenitor dysfunction to establish a niche for pulmonary fibrosis.

ATP-competitive partial antagonists of the IRE1α RNase segregate outputs of the UPR.

Stuck in a Moment: Does Abnormal Persistence of Epithelial Progenitors Drive Pulmonary Fibrosis?

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Vincent Auyeung, MD

Impaired Myofibroblast Proliferation is a Central Feature of Pathologic Post-Natal Alveolar Simplification.

BCL-2 Modulates IRE1α Activation to Attenuate ER Stress and Pulmonary Fibrosis.

IRE1α drives lung epithelial progenitor dysfunction to establish a niche for pulmonary fibrosis.

ATP-competitive partial antagonists of the IRE1α RNase segregate outputs of the UPR.

Stuck in a Moment: Does Abnormal Persistence of Epithelial Progenitors Drive Pulmonary Fibrosis?