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Thomas P. Mathews, PhD

@mathews-tom.bsky.social
74 followers 102 following 6 posts

Assistant Professor studying #metabolism and #lipidmetabolism; leading #massspectrometery at CRI at UTSW. #metabolomics #lipidomics Views are my own.

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Thomas P. Mathews, PhD @mathews-tom.bsky.social · 02/09/2026
These results suggest that consuming diets with a higher omega-3 to omega-6 ratio could improve the outcome of patients diagnosed with HO. Read the whole thing here! www.jci.org/articles/vie...
jci.org
JCI - Dietary omega-6 lipids promote postinjury aberrant bone formation in obesity
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Thomas P. Mathews, PhD @mathews-tom.bsky.social · 02/09/2026
Leveraging the metabolomics and lipidomics expertise of The Children’s Research Institute Metabolomics Facility, Stefanie and Ben were able to show that AA, derived from dietary LA, drives HO by increasing the production of prostaglandin and inflammation at the injury site.
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Thomas P. Mathews, PhD @mathews-tom.bsky.social · 02/09/2026
We worked with Stefanie Moye and Ben Levi in the UTSW Department of Surgery on a project to determine the metabolic underpinnings of heterotopic ossification (HO), a phenomenon characterized by the aberrant bone growth in soft tissue.
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Thomas P. Mathews, PhD @mathews-tom.bsky.social · 02/09/2026
For example, arachidonic acid (AA), an omega-6 fatty acid, can be converted into pro-inflammatory molecules like prostaglandin. In humans, much of the arachidonic acid in our bodies comes from omega-6 precursor linoleic acid (LA), which is enriched in western diets.
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Thomas P. Mathews, PhD @mathews-tom.bsky.social · 02/09/2026
You are what you eat! Omega-6 and omega-3 fatty acids are essential fatty acids, meaning we only get them from the foods we eat and our bodies need them to thrive. These fats are essential for maintaining the fluidity of cellular membranes, but they’re also powerful signaling molecules in the cell.
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Thomas P. Mathews, PhD @mathews-tom.bsky.social · 03/03/2026
Great paper from Shana Kelley’s group about how the elongation of fatty acids by ELOVL6 maintains membrane anchor points that activate pathogenic KRAS variants. An unexpected way that fatty acid metabolism regulates a yet “unbridgeable” oncogenic variant. Very cool. www.nature.com/articles/s41...
nature.com
ELOVL6 activity attenuation induces mutant KRAS degradation - Nature Chemical Biology
Inhibition of ELOVL6, a fatty acid elongation enzyme, selectively degrades mutant KRAS, disrupts its membrane localization and suppresses tumor growth, revealing a novel vulnerability in KRAS-driven c...
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