Cory Hogaboam

Professor

Cedars-Sinai Medical Center

United States

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About

Dr. Cory Hogaboam is a Professor at Cedars-Sinai Medical Center in the United States. His research primarily focuses on pulmonary fibrosis and the underlying mechanisms of lung diseases, with recent publications addressing anti-fibrotic therapies and their effects on lung tissue. He has contributed to the understanding of cellular interactions in interstitial lung disease and the role of inflammation in treatment strategies.

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University of Virginia Health System

UNITED STATES

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Cory Hogaboam

Research Interests

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About

Articles (20)

Caveolin Scaffolding Domain (CSD) Peptide LTI-2355 Modulates the Phagocytic and Synthetic Activity of Lung-Derived Myeloid Cells in Idiopathic Pulmonary Fibrosis (IPF) and Post-Acute Sequelae of COVID Fibrosis (PASC-F)

LTI-03 peptide demonstrates anti-fibrotic activity in ex vivo lung slices from patients with IPF

Evaluating Alveolar Regenerative Properties of Caveolin Scaffolding Peptides (CSD) in Three Dimensional (3D) Alveolospheres From IPF and Normal Donor Lung Samples

Pre-clinical Proof-of-Concept of Anti-fibrotic Activity of Caveolin-1 Scaffolding Domain Peptide LTI-03 in Ex Vivo Precision Cut Lung Slices From Patients With Idiopathic Pulmonary Fibrosis

Syndecan-1 Promotes Aberrant Transitional Epithelial Cell Accumulation During Lung Fibrosis

The FBXO45-GEF-H1 Axis Controls Germinal Center Formation and B-cell Lymphomagenesis.

RIOK2 transcriptionally regulates TRiC and dyskerin complexes to prevent telomere shortening

The Role of Inflammation and Fibrosis in Interstitial Lung Disease Treatment Decisions.

Immune mechanisms in fibrotic interstitial lung disease.

Interleukin 33 supports squamous cell carcinoma growth via a dual effect on tumour proliferation, migration and invasion, and T cell activation.

Reciprocal interactions between alveolar progenitor dysfunction and aging promote lung fibrosis.

Central lung gene expression associates with myofibroblast features in idiopathic pulmonary fibrosis

Potential mechanisms for lung fibrosis associated with COVID-19 infection

Epithelial plasticity and innate immune activation promote lung tissue remodeling following respiratory viral infection

Maladaptive TGF-b Signals to the Alveolar Epithelium Drive Fibrosis after COVID-19 Infection

Standard of care drugs do not modulate activity of senescent primary human lung fibroblasts

HER2 drives lung fibrosis by activating a metastatic cancer signature in invasive lung fibroblasts

Increased expression and accumulation of GDF15 in IPF extracellular matrix contribute to fibrosis

A Novel FBXO45-Gef-H1 Axis Controls Oncogenic Signaling in B-Cell Lymphoma

Sensitization of the UPR by loss of PPP1R15A promotes fibrosis and senescence in IPF

Collaborators (6)

Barry Stripp

Tanyalak Parimon

John Kim

Samuel Myers

Ting Xie

Catherine Bonham

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