Vincent C. Auyeung

Intensive Care Medicine
505 Parnassus Ave
San Francisco, CA 94143

Last Updated: 09/26/2026

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Found 16 publications

Alveolar Type II Cell-derived MMP1 high basal cells promote destructive microcysts in idiopathic pulmonary fibrosis.

Alveolar Type II Cell-derived MMP1 high basal cells promote destructive microcysts in idiopathic pulmonary fibrosis.

Journal: bioRxiv : the preprint server for biology
Published: January 23, 2026

Fibroblast orchestration of inflammaging via NF-kB activation.

Fibroblast orchestration of inflammaging via NF-kB activation.

Journal: bioRxiv : the preprint server for biology
Published: November 19, 2025

NF-κB-activated fibroblasts orchestrate inflammaging and emergence of pro-inflammatory granzyme K+ T cells.

NF-κB-activated fibroblasts orchestrate inflammaging and emergence of pro-inflammatory granzyme K+ T cells.

Journal: Immunity
Published: April 25, 2025

Myeloid-mesenchymal crosstalk drives ARG1-dependent profibrotic metabolism via ornithine in lung fibrosis.

Myeloid-mesenchymal crosstalk drives ARG1-dependent profibrotic metabolism via ornithine in lung fibrosis.

Journal: The Journal of clinical investigation
Published: January 16, 2025

Impaired myofibroblast proliferation is a central feature of pathologic post-natal alveolar simplification.

Impaired myofibroblast proliferation is a central feature of pathologic post-natal alveolar simplification.

Journal: eLife
Published: December 11, 2024

Senolytic-sensitive p16Ink4a+ fibroblasts in the tumor stroma rewire lung cancer metabolism and plasticity.

Senolytic-sensitive p16Ink4a+ fibroblasts in the tumor stroma rewire lung cancer metabolism and plasticity.

Journal: Cell stem cell
Published: October 26, 2024

Myeloid-mesenchymal crosstalk drives Arg1-dependent profibrotic metabolism via ornithine in lung fibrosis.

Myeloid-mesenchymal crosstalk drives Arg1-dependent profibrotic metabolism via ornithine in lung fibrosis.

Journal: bioRxiv : the preprint server for biology
Published: August 30, 2024

Pharmacologic inhibition of IRE1α-dependent decay protects alveolar epithelial identity and prevents pulmonary fibrosis in mice.

Pharmacologic inhibition of IRE1α-dependent decay protects alveolar epithelial identity and prevents pulmonary fibrosis in mice.

Journal: The Journal of clinical investigation
Published: July 09, 2024

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

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

Journal: bioRxiv : the preprint server for biology
Published: January 08, 2024

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

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

Journal: American journal of respiratory cell and molecular biology
Published: December 20, 2023

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

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

Journal: American journal of physiology. Lung cellular and molecular physiology
Published: February 16, 2022

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

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

Journal: Nature chemical biology
Published: December 26, 2020
Showing 1-12 of 16

Last Updated: 09/26/2026