期刊
CELL DEATH & DISEASE
卷 13, 期 7, 页码 -出版社
SPRINGERNATURE
DOI: 10.1038/s41419-022-05058-3
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资金
- Spanish Ministerio de Ciencia, Innovacion y Universidades/FEDER/UE [RTI2018-098645-B-100, PID2019-107948RA-I00, RYC-2017-21804]
- Agencia Espanola de Investigacion [PID2021-124096OB-I00, PID2021-126090OA-I00]
- Spanish Junta de Andalucia /FEDER/EU [P18-RT-1372]
- Spanish FEDER I+D+i-USE from University of Seville [US-1264806, US-1264152, US-1265062]
- Strategic Research Area MultiPark (Multidisciplinary Research focused on neurodegenerative diseases) at Lund University
- Swedish Alzheimer foundation
- Swedish Brain Foundation
- Crafoord Foundation
- Swedish Dementia Association
- G&J Kock Foundation
- Olle Engkvist Foundation
- Swedish Research Council [2019-06333]
- Royal Physiographic Society [42222, 40594]
- A.E. Berger Foundation
- Swedish Parkinson Foundation
- Medical Faculty at Lund University
- Swedish Research Council [2019-06333] Funding Source: Swedish Research Council
The high-throughput single-cell transcriptomic analysis technique has revealed common characteristics of galectin-3 upregulation in disease-associated microglia. The ability of galectin-3 to interact with key pattern recognition receptors has been demonstrated, and increasing evidence supports its involvement in major neurodegenerative diseases.
The advent of high-throughput single-cell transcriptomic analysis of microglia has revealed different phenotypes that are inherently associated with disease conditions. A common feature of some of these activated phenotypes is the upregulation of galectin-3. Representative examples of these phenotypes include disease-associated microglia (DAM) and white-associated microglia (WAM), whose role(s) in neuroprotection/neurotoxicity is a matter of high interest in the microglia community. In this review, we summarise the main findings that demonstrate the ability of galectin-3 to interact with key pattern recognition receptors, including, among others, TLR4 and TREM2 and the importance of galectin-3 in the regulation of microglia activation. Finally, we discuss increasing evidence supporting the involvement of this lectin in the main neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, traumatic brain injury, and stroke.
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