Multi-omic and multispecies analysis of right ventricular dysfunction.

RV cardiac MRI comparative study proteomics transcriptomics

Journal

The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation
ISSN: 1557-3117
Titre abrégé: J Heart Lung Transplant
Pays: United States
ID NLM: 9102703

Informations de publication

Date de publication:
01 Oct 2023
Historique:
received: 07 04 2023
revised: 14 09 2023
accepted: 28 09 2023
pubmed: 3 10 2023
medline: 3 10 2023
entrez: 2 10 2023
Statut: aheadofprint

Résumé

Right ventricular failure (RVF) is a leading cause of morbidity and mortality in multiple cardiovascular diseases, but there are no treatments for RVF as therapeutic targets are not clearly defined. Contemporary transcriptomic/proteomic evaluations of RVF are predominately conducted in small animal studies, and data from large animal models are sparse. Moreover, a comparison of the molecular mediators of RVF across species is lacking. Transcriptomics and proteomics analyses defined the pathways associated with cardiac magnetic resonance imaging (MRI)-derived values of RV hypertrophy, dilation, and dysfunction in control and pulmonary artery banded (PAB) pigs. Publicly available data from rat monocrotaline-induced RVF and pulmonary arterial hypertension patients with preserved or impaired RV function were used to compare molecular responses across species. PAB pigs displayed significant right ventricle/ventricular (RV) hypertrophy, dilation, and dysfunction as quantified by cardiac magnetic resonance imaging. Transcriptomic and proteomic analyses identified pathways associated with RV dysfunction and remodeling in PAB pigs. Surprisingly, disruptions in fatty acid oxidation (FAO) and electron transport chain (ETC) proteins were different across the 3 species. FAO and ETC proteins and transcripts were mostly downregulated in rats but were predominately upregulated in PAB pigs, which more closely matched the human response. All species exhibited similar dysregulation of the dilated cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy pathways. The porcine metabolic molecular signature was more similar to human RVF than rodents. These data suggest there may be divergent molecular responses of RVF across species, and pigs may more accurately recapitulate metabolic aspects of human RVF.

Sections du résumé

BACKGROUND BACKGROUND
Right ventricular failure (RVF) is a leading cause of morbidity and mortality in multiple cardiovascular diseases, but there are no treatments for RVF as therapeutic targets are not clearly defined. Contemporary transcriptomic/proteomic evaluations of RVF are predominately conducted in small animal studies, and data from large animal models are sparse. Moreover, a comparison of the molecular mediators of RVF across species is lacking.
METHODS METHODS
Transcriptomics and proteomics analyses defined the pathways associated with cardiac magnetic resonance imaging (MRI)-derived values of RV hypertrophy, dilation, and dysfunction in control and pulmonary artery banded (PAB) pigs. Publicly available data from rat monocrotaline-induced RVF and pulmonary arterial hypertension patients with preserved or impaired RV function were used to compare molecular responses across species.
RESULTS RESULTS
PAB pigs displayed significant right ventricle/ventricular (RV) hypertrophy, dilation, and dysfunction as quantified by cardiac magnetic resonance imaging. Transcriptomic and proteomic analyses identified pathways associated with RV dysfunction and remodeling in PAB pigs. Surprisingly, disruptions in fatty acid oxidation (FAO) and electron transport chain (ETC) proteins were different across the 3 species. FAO and ETC proteins and transcripts were mostly downregulated in rats but were predominately upregulated in PAB pigs, which more closely matched the human response. All species exhibited similar dysregulation of the dilated cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy pathways.
CONCLUSIONS CONCLUSIONS
The porcine metabolic molecular signature was more similar to human RVF than rodents. These data suggest there may be divergent molecular responses of RVF across species, and pigs may more accurately recapitulate metabolic aspects of human RVF.

Identifiants

pubmed: 37783299
pii: S1053-2498(23)02056-9
doi: 10.1016/j.healun.2023.09.020
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NHLBI NIH HHS
ID : R01 HL158795
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL162927
Pays : United States

Commentaires et corrections

Type : UpdateOf

Informations de copyright

Copyright © 2023 International Society for the Heart and Lung Transplantation. Published by Elsevier Inc. All rights reserved.

Auteurs

Jenna B Mendelson (JB)

Department of Integrative Biology and Physiology, University of Minnesota, Minneapolis, Minnesota.

Jacob D Sternbach (JD)

Department of Medicine, Lillehei Heart Institute, University of Minnesota, Minneapolis, Minnesota.

Michelle J Doyle (MJ)

Department of Medicine, Lillehei Heart Institute, University of Minnesota, Minneapolis, Minnesota.

Lauren Mills (L)

Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota.

Lynn M Hartweck (LM)

Department of Medicine, Lillehei Heart Institute, University of Minnesota, Minneapolis, Minnesota.

Walt Tollison (W)

Department of Surgery, Experimental Surgical Services Laboratory, University of Minnesota, Minneapolis, Minnesota.

John P Carney (JP)

Department of Surgery, Experimental Surgical Services Laboratory, University of Minnesota, Minneapolis, Minnesota.

Matthew T Lahti (MT)

Department of Surgery, Experimental Surgical Services Laboratory, University of Minnesota, Minneapolis, Minnesota.

Richard W Bianco (RW)

Department of Surgery, Experimental Surgical Services Laboratory, University of Minnesota, Minneapolis, Minnesota.

Rajat Kalra (R)

Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, Minnesota.

Felipe Kazmirczak (F)

Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, Minnesota.

Charles Hindmarch (C)

Queen's Cardiopulmonary Unit, Department of Medicine, Queen's University, Kingston, Ontario, Canada.

Stephen L Archer (SL)

Queen's Cardiopulmonary Unit, Department of Medicine, Queen's University, Kingston, Ontario, Canada.

Kurt W Prins (KW)

Department of Medicine, Lillehei Heart Institute, University of Minnesota, Minneapolis, Minnesota; Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, Minnesota. Electronic address: prin0088@umn.edu.

Cindy M Martin (CM)

DeBakey Heart and Vascular Center, Houston Methodist, Houston, Texas.

Classifications MeSH