Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2024 Oct 31;38(20):e70130.
doi: 10.1096/fj.202402126R.

LC3-associated phagocytosis and human diseases: Insights from mechanisms to therapeutic potential

Affiliations
Review

LC3-associated phagocytosis and human diseases: Insights from mechanisms to therapeutic potential

Xu Chen et al. FASEB J. .

Abstract

LC3-associated phagocytosis (LAP) is a distinct type of autophagy that involves the sequestration of extracellular material by phagocytes. Beyond the removal of dead cells and cellular debris from eukaryotic cells, LAP is also involved in the removal of a variety of pathogens, including bacteria, fungi, and viruses. These events are integral to multiple physiological and pathological processes, such as host defense, inflammation, and tissue homeostasis. Dysregulation of LAP has been associated with the pathogenesis of several human diseases, including infectious diseases, autoimmune diseases, and neurodegenerative diseases. Thus, understanding the molecular mechanisms underlying LAP and its involvement in human diseases may provide new insights into the development of novel therapeutic strategies for these conditions. In this review, we summarize and highlight the current consensus on the role of LAP and its biological functions in disease progression to propose new therapeutic strategies. Further studies are needed to illustrate the precise role of LAP in human disease and to determine new therapeutic targets for LAP-associated pathologies.

Keywords: LAP‐associated pathology; LC3‐associated phagocytosis; molecular mechanism; therapeutic strategy.

PubMed Disclaimer

References

REFERENCES

    1. Tsukada M, Ohsumi Y. Isolation and characterization of autophagy‐defective mutants of Saccharomyces cerevisiae. FEBS Lett. 1993;333:169‐174.
    1. Levine B, Kroemer G. Biological functions of autophagy genes: a disease perspective. Cell. 2019;176:11‐42.
    1. Nie T, Zhu L, Yang Q. The classification and basic processes of autophagy. Adv Exp Med Biol. 2021;1208:3‐16.
    1. Köster S, Upadhyay S, Chandra P, et al. Mycobacterium tuberculosis is protected from NADPH oxidase and LC3‐associated phagocytosis by the LCP protein CpsA. Proc Natl Acad Sci USA. 2017;114:E8711‐E8720.
    1. Chen Y, He Y, Wu X, et al. Rubicon promotes the M2 polarization of Kupffer cells via LC3‐associated phagocytosis‐mediated clearance to improve liver transplantation. Cell Immunol. 2022;378:104556.

Substances

LinkOut - more resources