Lung emphysema and impaired macrophage elastase clearance in mucolipin 3 deficient mice.
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
14 01 2022
14 01 2022
Historique:
received:
17
03
2021
accepted:
16
12
2021
entrez:
15
1
2022
pubmed:
16
1
2022
medline:
17
2
2022
Statut:
epublish
Résumé
Lung emphysema and chronic bronchitis are the two most common causes of chronic obstructive pulmonary disease. Excess macrophage elastase MMP-12, which is predominantly secreted from alveolar macrophages, is known to mediate the development of lung injury and emphysema. Here, we discovered the endolysosomal cation channel mucolipin 3 (TRPML3) as a regulator of MMP-12 reuptake from broncho-alveolar fluid, driving in two independently generated Trpml3
Identifiants
pubmed: 35031603
doi: 10.1038/s41467-021-27860-x
pii: 10.1038/s41467-021-27860-x
pmc: PMC8760276
doi:
Substances chimiques
Mcoln3 protein, mouse
0
Transient Receptor Potential Channels
0
Pancreatic Elastase
EC 3.4.21.36
Matrix Metalloproteinase 12
EC 3.4.24.65
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
318Subventions
Organisme : NIDCD NIH HHS
ID : R01 DC015903
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK111032
Pays : United States
Informations de copyright
© 2022. The Author(s).
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