NGF and Its Role in Immunoendocrine Communication during Metabolic Syndrome.
TrkA
adipocytes
metabolic diseases
metabolic homeostasis
metabolism
neurotrophin
p75NTR
pancreatic beta cell
sex steroid hormones
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:
19 Jan 2023
19 Jan 2023
Historique:
received:
25
11
2022
revised:
18
12
2022
accepted:
19
12
2022
entrez:
11
2
2023
pubmed:
12
2
2023
medline:
15
2
2023
Statut:
epublish
Résumé
Nerve growth factor (NGF) was the first neurotrophin described. This neurotrophin contributes to organogenesis by promoting sensory innervation and angiogenesis in the endocrine and immune systems. Neuronal and non-neuronal cells produce and secrete NGF, and several cell types throughout the body express the high-affinity neurotrophin receptor TrkA and the low-affinity receptor p75NTR. NGF is essential for glucose-stimulated insulin secretion and the complete development of pancreatic islets. Plus, this factor is involved in regulating lipolysis and thermogenesis in adipose tissue. Immune cells produce and respond to NGF, modulating their inflammatory phenotype and the secretion of cytokines, contributing to insulin resistance and metabolic homeostasis. This neurotrophin regulates the synthesis of gonadal steroid hormones, which ultimately participate in the metabolic homeostasis of other tissues. Therefore, we propose that this neurotrophin's imbalance in concentrations and signaling during metabolic syndrome contribute to its pathophysiology. In the present work, we describe the multiple roles of NGF in immunoendocrine organs that are important in metabolic homeostasis and related to the pathophysiology of metabolic syndrome.
Identifiants
pubmed: 36768281
pii: ijms24031957
doi: 10.3390/ijms24031957
pmc: PMC9916855
pii:
doi:
Substances chimiques
Nerve Growth Factor
9061-61-4
NGF protein, human
0
Receptor, Nerve Growth Factor
0
Receptor, trkA
EC 2.7.10.1
Receptors, Nerve Growth Factor
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : PAPIIT, DGAPA UNAM
ID : IN208720
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