The Brain-Heart Axis: Neuroinflammatory Interactions in Cardiovascular Disease.
Arrhythmia-related stroke
Cardiometabolic syndrome
Cardiovascular neurogenic aging
Heart brain axis
Neuroinflammatory interactions
Stress cardiomyopathy
Journal
Current cardiology reports
ISSN: 1534-3170
Titre abrégé: Curr Cardiol Rep
Pays: United States
ID NLM: 100888969
Informations de publication
Date de publication:
12 2023
12 2023
Historique:
accepted:
30
10
2023
pmc-release:
01
12
2024
medline:
26
1
2024
pubmed:
23
11
2023
entrez:
23
11
2023
Statut:
ppublish
Résumé
The role of neuroimmune modulation and inflammation in cardiovascular disease has been historically underappreciated. Physiological connections between the heart and brain, termed the heart-brain axis (HBA), are bidirectional, occur through a complex network of autonomic nerves/hormones and cytokines, and play important roles in common disorders. At the molecular level, advances in the past two decades reveal complex crosstalk mediated by the sympathetic and parasympathetic nervous systems, the renin-angiotensin aldosterone and hypothalamus-pituitary axes, microRNA, and cytokines. Afferent pathways amplify proinflammatory signals via the hypothalamus and brainstem to the periphery, promoting neurogenic inflammation. At the organ level, while stress-mediated cardiomyopathy is the prototypical disorder of the HBA, cardiac dysfunction can result from a myriad of neurologic insults including stroke and spinal injury. Atrial fibrillation is not necessarily a causative factor for cardioembolic stroke, but a manifestation of an abnormal atrial substrate, which can lead to the development of stroke independent of AF. Central and peripheral neurogenic proinflammatory factors have major roles in the HBA, manifesting as complex bi-directional relationships in common conditions such as stroke, arrhythmia, and cardiomyopathy.
Identifiants
pubmed: 37994952
doi: 10.1007/s11886-023-01990-8
pii: 10.1007/s11886-023-01990-8
pmc: PMC10908342
mid: NIHMS1969671
doi:
Substances chimiques
Cytokines
0
Types de publication
Journal Article
Review
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
1745-1758Subventions
Organisme : NIA NIH HHS
ID : P30 AG021342
Pays : United States
Organisme : NIA NIH HHS
ID : R03 AG074067
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001863
Pays : United States
Informations de copyright
© 2023. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.
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