ENaC x Mucin

Last update 08 May 2025

Basic Info

Related Targets

ENaCMucin

Drugs associated with ENaC x Mucin

VS-024

Target

ENaC x Mucin

Mechanism

ENaC modulators [+2]

Active Org.

Nuvara Therapeutics

Originator Org.

University of Florida Research Foundation, Inc.

Active Indication

Pulmonary Disease, Chronic Obstructive

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ENaC x Mucin

100 Translational Medicine associated with ENaC x Mucin

0 Patents (Medical) associated with ENaC x Mucin

Literatures (Medical) associated with ENaC x Mucin

01 Mar 2025·American Journal of Physiology-Cell Physiology

Modeling ocular surface ion and water transport by generation of lipid- and mucin-producing human meibomian gland and conjunctival epithelial cells

Article

Author: Leveziel, Nicolas ; Cantereau, Anne ; Terrasse, Gaëtan ; Bur, Catherine ; Becq, Frédéric ; Flausse, Roxane ; Barrault, Christine ; Radji, Chloë

We generated human meibomian gland and conjunctival epithelial cells producing lipids and mucins. We identified ion channels including ENaC, CFTR, TMEM16a, and KCNQ1, as well as NKCC. We found that electrolyte and water flux are regulated by signaling pathways mediated by purinergic and VIP receptors. Our findings provide valuable insights into epithelial ion and water transport in the human conjunctiva and meibomian gland, enhancing understanding of these processes in both physiological and disease states.

15 Sep 2020·The Journal of ImmunologyQ2 · MEDICINE

The Innate Lymphoid System Is a Critical Player in the Manifestation of Mucoinflammatory Airway Disease in Mice

Q2 · MEDICINE

Article

Author: Deshane, Jessy S ; Boucher, Richard C ; Choudhary, Ishita ; Wang, Yong ; Paudel, Kshitiz ; Sharma, Rahul ; Mao, Yun ; Lewis, Brandon W ; Patial, Sonika ; Saini, Yogesh

AbstractInnate lymphoid and adaptive immune cells are known to regulate epithelial responses, including mucous cell metaplasia (MCM), but their roles in mucoinflammatory airway diseases, such as cystic fibrosis, remain unknown. Scnn1b transgenic (Scnn1b-Tg+) mice, which recapitulate cystic fibrosis–like mucoinflammatory airway disease, deficient in innate lymphoid (Il2rg knockout mice [Il2rgKO]), adaptive immune (Rag1 knockout mice [Rag1KO]), or both systems (Il2rgKO/Rag1KO), were employed to investigate their respective contributions in the pathogenesis of mucoinflammatory airway disease. As previously reported, immunocompetent Tg+ juveniles exhibited spontaneous neonatal bacterial infections with robust mucoinflammatory features, including elevated expression of Th2-associated markers accompanied by MCM, elevated MUC5B expression, and airway mucus obstruction. The bacterial burden was increased in Il2rgKO/Tg+ juveniles but returned to significantly lower levels in Il2rgKO/Rag1KO/Tg+ juveniles. Mechanistically, this improvement reflected reduced production of adaptive immunity-derived IL-10 and, in turn, increased activation of macrophages. Although all the mucoinflammatory features were comparable between the immunocompetent Tg+ and Rag1KO/Tg+ juveniles, the Il2rgKO/Tg+ and Il2rgKO/Rag1KO/Tg+ juveniles exhibited suppressed expression levels of Th2 markers, diminished MCM, suppressed MUC5B expression, and reduced mucus obstruction. Collectively, these data indicate that, in the context of airway mucus obstruction, the adaptive immune system suppresses antibacterial macrophage activation, whereas the innate lymphoid system contributes to MCM, mucin production, and mucus obstruction.

15 Mar 2020·The Journal of ImmunologyQ2 · MEDICINE

Ablation of IL-33 Suppresses Th2 Responses but Is Accompanied by Sustained Mucus Obstruction in the Scnn1b Transgenic Mouse Model

Q2 · MEDICINE

Article

Author: Vo, Thao ; Choudhary, Ishita ; Kidder, Allison ; Saini, Yogesh ; Patial, Sonika ; Wakamatsu, Nobuko ; Lewis, Brandon W ; Bathula, Chandra ; Ehre, Camille

AbstractCystic fibrosis is characterized by dehydration of the airway surface liquid layer with persistent mucus obstruction. Th2 immune responses are often manifested as increased mucous cell density (mucous cell metaplasia) associated with mucus obstruction. IL-33 is a known inducer of Th2 immune responses, but its roles in mucus obstruction and related phenotypes in a cystic fibrosis–like lung disease model (i.e., Scnn1b-Tg–positive [Tg+]) mouse, remain unclear. Accordingly, IL-33 knockout (IL-33KO) Tg+ mice were examined and compared with IL-33 heterozygous (IL-33HET) Tg+ mice. As compared with IL-33HET/Tg+ mice, IL-33KO/Tg+ mice had complete absence of bronchoalveolar lavage fluid eosinophilia, accompanied with significant reduction in bronchoalveolar lavage fluid concentration of IL-5, a cytokine associated with eosinophil differentiation and recruitment, and IL-4, a major Th2 cytokine. As compared with IL-33HET/Tg+ mice, IL-33KO/Tg+ mice had significantly reduced levels of Th2-associated gene signatures (Slc26a4, Clca1, Retnla, and Chi3l4), along with complete loss of intracellular mucopolysaccharide staining in the airway epithelium. As compared with IL-33HET/Tg+ mice, although the IL-33KO/Tg+ mice had significantly reduced levels of MUC5AC protein expression, they showed no reduction in the degree of mucus obstruction, MUC5B protein expression, bacterial burden, and neonatal mortality. Interestingly, the histological features, including subepithelial airway inflammation and alveolar space enlargement, were somewhat exaggerated in IL-33KO/Tg+ mice compared with IL-33HET/Tg+ mice. Taken together, our data indicate that although IL-33 modulates Th2 inflammatory responses and MUC5AC protein production, mucus obstruction is not dependent on IL-33.

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