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Editorial
. 2025 Apr-May;29(4-5):185-188.
doi: 10.1080/14728222.2025.2500416. Epub 2025 May 2.

LPAR5 as a prospective therapeutic target for treating microvillus inclusion disease

Andreanna Burman  1   2 , Izumi Kaji  1   2   3
Affiliations
Editorial

LPAR5 as a prospective therapeutic target for treating microvillus inclusion disease

Andreanna Burman et al. Expert Opin Ther Targets. 2025 Apr-May.
No abstract available

Keywords: Congenital diarrhea and enteropathy (CODE); enteroid; lysophosphatidic acid; mouse model; small intestine.

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Conflict of interest statement

Declaration of interest

I Kaji is a named inventor on a patent application related to this research and owned by the Vanderbilt University. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

References

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    1. Momoh M, Rathan-Kumar S, Burman A, et al. Alterations in cellular metabolic pathway and epithelial cell maturation induced by MYO5B defects are partially reversible by LPAR5 activation. Am J Physiol Gastrointest Liver Physiol. (2024) - PMC - PubMed
    1. Roland JT, Bryant DM, Datta A, et al. Rab GTPase-Myo5B complexes control membrane recycling and epithelial polarization. Proc Natl Acad Sci U S A. (2011) - PMC - PubMed
    1. Engevik AC, Kaji I, Engevik MA, et al. Loss of MYO5B Leads to Reductions in Na(+) Absorption With Maintenance of CFTR-Dependent Cl(−) Secretion in Enterocytes. Gastroenterology. (2018) - PMC - PubMed
    1. Weis VG, Knowles BC, Choi E, et al. Loss of MYO5B in mice recapitulates Microvillus Inclusion Disease and reveals an apical trafficking pathway distinct to neonatal duodenum. Cell Mol Gastroenterol Hepatol. (2016) - PMC - PubMed

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