Update on the Role of β2AR and TRPV1 in Respiratory Diseases.
COPD
RSV
TRPV1
asthma
bronchiolitis
cystic fibrosis
respiratory diseases
β2AR
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
24 Sep 2024
24 Sep 2024
Historique:
received:
24
08
2024
revised:
16
09
2024
accepted:
23
09
2024
medline:
16
10
2024
pubmed:
16
10
2024
entrez:
16
10
2024
Statut:
epublish
Résumé
Respiratory diseases (RDs) constitute a common public health problem both in industrialized and developing countries. The comprehension of the pathophysiological mechanisms underlying these conditions and the development of new therapeutic strategies are critical for improving the quality of life of affected patients. β2-adrenergic receptor (β2AR) and transient receptor potential vanilloid 1 (TRPV1) are both involved in physiological responses in the airways. β2AR is implicated in bronchodilation, mucociliary clearance, and anti-inflammatory effects, while TRPV1 is involved in the mediation of pain and cough reflexes. In RDs, such as respiratory infections, asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis, the concentration and expression of these receptors can be altered, leading to significant consequences. In this review, we provided an update on the literature about the role of β2AR and TRPV1 in these conditions. We reported how the diminished or defective expression of β2AR during viral infections or prolonged therapy with β2-agonists can increase the severity of these pathologies and impact the prognosis. Conversely, the role of TRPV1 was pivotal in neuroinflammation, and its modulation could lead to innovative treatment strategies in specific patients. We indicate future perspectives and potential personalized treatments in RDs through a comprehensive analysis of the roles of these receptors in the physiological and pathological mechanisms of these pathologies.
Identifiants
pubmed: 39408565
pii: ijms251910234
doi: 10.3390/ijms251910234
pii:
doi:
Substances chimiques
TRPV Cation Channels
0
TRPV1 protein, human
0
Receptors, Adrenergic, beta-2
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM