REVIEW article
Front. Immunol.
Sec. Autoimmune and Autoinflammatory Disorders : Autoimmune Disorders
This article is part of the Research TopicThe Role of Innate Immunity in the Pathogenesis of Autoimmune and Autoinflammatory DiseasesView all 9 articles
The Research Progress of LACC1
Provisionally accepted
- 1Kunming Medical University, Kunming, China
- 2First Affiliated Hospital of Kunming Medical University, Kunming, China
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Laccase Domain-Containing 1（LACC1）is highly expressed in myeloid macrophages, and plays a crucial role in coordinating innate and adaptive immune responses by integrating lipid, polyamine, and purine metabolism pathways. This study comprehensively discusses the molecular structure, enzymatic functions, and signaling pathways associated with LACC1. Notably, the M-CSF/AKT/mTOR/LACC1 pathway primarily regulates cellular autophagy. Additionally, the PPARα/RXR/PPRE/LACC1, miR-211-5p/KDM2B/LACC1, LACC1/AMPK/NLRP3, LACC1/NF-kB, LACC1/MAPK, LACC1/ROS/NOD2/PIPK2, LACC1/JAK-STAT, and LACC1/CCL5 signaling pathways are significantly involved in modulating inflammatory responses. Furthermore, the article provides a comprehensive summary of the pathogenic mechanisms and recent advancements in research concerning LACC1 in immune diseases, metabolic disorders, infectious diseases, and neurological conditions. In conclusion, LACC1 serves as a pivotal immune-metabolic hub, offering new insights and potential therapeutic targets for the study of related diseases.
Keywords: LACC1, Inflammation, immune, signaling pathway, Diseases
Received: 04 Sep 2025; Accepted: 03 Nov 2025.
Copyright: © 2025 Li, Cui, Yang, Nie, Wang and sun. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: shibo sun, shibosunky@126.com
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