Searching the Resource Information Network

Our searching services are busy right now. Please try again later

  • Register
X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

X

Leaving Community

Are you sure you want to leave this community? Leaving the community will revoke any permissions you have been granted in this community.

No
Yes

Esomeprazole attenuates inflammatory and fibrotic response in lung cells through the MAPK/Nrf2/HO1 pathway.

Afshin Ebrahimpour | Min Wang | Li Li | Anil G Jegga | Mark D Bonnen | N Tony Eissa | Ganesh Raghu | Soma Jyothula | Farrah Kheradmand | Nicola A Hanania | Ivan O Rosas | Yohannes T Ghebre
Journal of inflammation (London, England) | 2021

Idiopathic pulmonary fibrosis (IPF) is an orphan disease characterized by progressive loss of lung function resulting in shortness of breath and often death within 3-4 years of diagnosis. Repetitive lung injury in susceptible individuals is believed to promote chronic oxidative stress, inflammation, and uncontrolled collagen deposition. Several preclinical and retrospective clinical studies in IPF have reported beneficial outcomes associated with the use of proton pump inhibitors (PPIs) such as esomeprazole. Accordingly, we sought to investigate molecular mechanism(s) by which PPIs favorably regulate the disease process.

Pubmed ID: 34011367

Research resources used in this publication

None found

Antibodies used in this publication

None found

Associated grants

  • Agency: NHLBI NIH HHS, United States
    Id: K01HL118683
  • Agency: NHLBI NIH HHS, United States
    Id: R01HL137703
  • Agency: NHLBI NIH HHS, United States
    Id: T32HL007747-22
  • Agency: NIAMS NIH HHS, United States
    Id: R56AR077445

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.

This is a list of tools and resources that we have found mentioned in this publication.


LINCS Connectivity Map (tool)

RRID:SCR_002639

A catalog of gene-expression data collected from human cells treated with chemical compounds and genetic reagents. Computational methods to reduce the number of necessary genomic measurements along with streamlined methodologies enable the current effort to significantly increase the size of the CMap database and along with it, our potential to connect human diseases with the genes that underlie them and the drugs that treat them. The NIH has funded a large expansion of the Connectivity Map dataset through the Library of Integrated Network-based Cellular Signatures (LINCS). The Broad Institute's LINCS center aims to create a first installment of data generation and analysis for the LINCS program. Through these data LINCS intends to accelerate the discovery process by systematically revealing connections between genes/compounds discovered in screens and molecular pathways that underlie disease states.

View all literature mentions

Cytoscape (tool)

RRID:SCR_003032

Software platform for complex network analysis and visualization. Used for visualization of molecular interaction networks and biological pathways and integrating these networks with annotations, gene expression profiles and other state data.

View all literature mentions

KEGG (tool)

RRID:SCR_012773

Integrated database resource consisting of 16 main databases, broadly categorized into systems information, genomic information, and chemical information. In particular, gene catalogs in completely sequenced genomes are linked to higher-level systemic functions of cell, organism, and ecosystem. Analysis tools are also available. KEGG may be used as reference knowledge base for biological interpretation of large-scale datasets generated by sequencing and other high-throughput experimental technologies.

View all literature mentions