LGALS3BP Induces Insulin Resistance via TLR2-IKKα/β Pathway-Mediated IRS1 Serine Phosphorylation
LGALS3BP contributes to IR through inflammatory responses, particularly via TLR2-IKKα/β signaling that regulates IRS1 serine phosphorylation. LGALS3BP deficiency improves insulin sensitivity and reduces inflammation, suggesting that targeting LGALS3BP may represent a potential therapeutic strategy for metabolic disorders such as T2D and MASLD.
Authors
- Jun-Eul Hwang
- Eun Gene Sun (ORCID: https://orcid.org/0000-0002-3396-6966)
- Woo Kyun Bae (ORCID: https://orcid.org/0000-0003-0267-1943)
- Ik‐Joo Chung (ORCID: https://orcid.org/0000-0003-0479-8067)
- Hyun-Jeong Shim (ORCID: https://orcid.org/0000-0001-7450-7822)
- Dae‐Hwan Kim (ORCID: https://orcid.org/0000-0001-8746-6177)
- Sanghee Cho (ORCID: https://orcid.org/0000-0001-6715-9348)
- Minjeong Sung
Institutions
- Chonnam National University Hwasun Hospital (KR)
Publication Details
- Journal
- Endocrinology and Metabolism
- Published
- 2025-10-22
- DOI
- https://doi.org/10.3803/enm.2025.2448
- Citations
- 2
- Primary Topic
- NF-κB Signaling Pathways
- Type
- article
- Field-Weighted Citation Impact
- 1.87
Funders
- Mike and Josie Harper Cancer Research Institute
- National Research Foundation
- Chonnam National University
- Ministry of Science and ICT, South Korea
- Chonnam National University Hwasun Hospital