The Monocrotaline Rat Model of Right Heart Disease Induced by Pulmonary Artery Hypertension.

cardiomyocyte excitation–contraction coupling monocrotaline pulmonary artery hypertension right heart failure right ventricular hypertrophy

Journal

Biomedicines
ISSN: 2227-9059
Titre abrégé: Biomedicines
Pays: Switzerland
ID NLM: 101691304

Informations de publication

Date de publication:
23 Aug 2024
Historique:
received: 24 07 2024
revised: 16 08 2024
accepted: 17 08 2024
medline: 28 9 2024
pubmed: 28 9 2024
entrez: 28 9 2024
Statut: epublish

Résumé

Pulmonary artery hypertension (PAH) is characterised by increased pulmonary vascular resistance (PVR) resulting in elevated pressure in the pulmonary artery supplying the pulmonary circulation. Disease of the right ventricle (RV) often manifests as a result of PAH placing excessive pressure on the right side of the heart. Although a relatively rare disease in humans, the impact of sustained PAH is severe, with poor outcomes even in treated individuals. As PAH develops, the blood flow is restricted through the pulmonary arteries and the right ventricle hypertrophies due to the increased strain of pumping blood through the pulmonary circulation. With time, RV hypertrophy progresses to right heart failure, impacting the supply of blood to the left ventricle and systemic circulation. Although right heart failure can currently be treated, it cannot be cured. There is therefore a need for more research into the physiological changes that cause the heart to fail under pressure overload. This review aims to evaluate the monocrotaline (MCT) rat model of PAH as a means of studying the cellular mechanisms associated with the development of RV hypertrophy and right heart failure.

Identifiants

pubmed: 39335458
pii: biomedicines12091944
doi: 10.3390/biomedicines12091944
pii:
doi:

Types de publication

Journal Article Review

Langues

eng

Subventions

Organisme : Auckland Medical Research Foundation, New Zealand
ID : 1121010, and 1124006
Organisme : The National Heart Foundation of New Zealand
ID : Fellowship 1873
Organisme : Maurice & Phyllis Paykel Trust, New Zealand
ID : 231109

Auteurs

Anna Maria Krstic (AM)

Department of Physiology, University of Auckland, Auckland 1142, New Zealand.

Timothy L M Jones (TLM)

Department of Physiology, University of Auckland, Auckland 1142, New Zealand.
Division of Cardiology, Anschutz Medical Campus, University of Colorado, Aurora, CO 80045, USA.

Amelia S Power (AS)

Department of Physiology, University of Auckland, Auckland 1142, New Zealand.

Marie-Louise Ward (ML)

Department of Physiology, University of Auckland, Auckland 1142, New Zealand.

Classifications MeSH