Adam Lab
Our Mission
Our Mission is to find novel therapeutics to treat tissue damage and organ dysfunction caused by disproportionate inflammatory responses. We aim to achieve that by identifying the most critical mechanisms of the pathophysiology that lead to chronic and excessive inflammation.
September 2024 - We are happy to announce our new NIGMS R35 award!
July 2024 - Shuhan's paper was published in Neuroscience!
June 2024 - Congrats Ramon on your AHA CDA award. Looking forward to continue working with you as part of your mentorship team!
January 2024 - Our Phase I trial showing safety of topical trametinib for rosacea was published!
September 2023 - So proud of Ramon! He just published his work on endothelial epigenetic response to shock, was promoted to assistant professor, and started a bioinformatics core!
August 2022 - Nina is on roll! She just published her data showing an autocrine IL-6 signaling loop in endothelial cells. Read here!
July 2021 - Congrats Nina for your first author publication showing the crucial roles for endothelial SOCS3!
June 2020 - Shuhan Lu is our new PhD student! Welcome!
May 2020 - Busy month! Thank you NIGMS for supporting the purchase of a Heidelberg Spectralis HRA+OCT2 for our critical illness models!
May 2020 - First data from very sick COVID19 patients show that very high CCL19 is associated with poor outcome. Read here!
May 2019 - Kevin Lau was awarded the 2019 AΩA Carolyn L. Kuckein Student Research Fellowship!
March 2019 - Congratulations Dr Hiba Alsaffar! Great job Hiba defending your Thesis!
Our research - When inflammation goes awry
A cytokine-driven acute increase in vascular permeability is an essential feature of the inflammatory response leading to tissue repair and pathogen clearance. However, sustained vascular leakage due to prolonged or exacerbated inflammation leads to organ damage, lasting sequelae and increased mortality. The mechanism mediating the acute (minutes to hours) responses to proinflammatory cytokine signaling are well-described: phosphorylation of tyrosines in adherens junction proteins and an increase in actin-myosin contractility are two main mechanisms leading to a quick loss of endothelial intercellular adhesion and thus an increase in vascular permeability. Despite its importance in severe and chronic inflammation, little is known about the changes in the endothelium causing a sustained (lasting hours to days) vascular barrier breakdown. Understanding these long-term mechanisms may prove crucial to allow us to directly target vascular leakage and minimize tissue damage, thus reducing the rates of mortality and chronic sequelae of excessive edema.
Click on any picture to learn more about our research program:
Funding
We are grateful for our current and past funding from:
