Endothelial-Mesenchymal Transition in Heart Failure With a Preserved Ejection Fraction: Insights Into the Cardiorenal Syndrome.


Journal

Circulation. Heart failure
ISSN: 1941-3297
Titre abrégé: Circ Heart Fail
Pays: United States
ID NLM: 101479941

Informations de publication

Date de publication:
09 2021
Historique:
pubmed: 20 8 2021
medline: 24 12 2021
entrez: 19 8 2021
Statut: ppublish

Résumé

The management of clinical heart failure with a preserved ejection fraction (HFpEF) is often complicated by concurrent renal dysfunction, known as the cardiorenal syndrome. This, combined with the notable lack of evidence-based therapies for HFpEF, highlights the importance of examining mechanisms and targetable pathways in HFpEF with the cardiorenal syndrome. HFpEF was induced in mice by uninephrectomy, infusion of Kidneys from HFpEF mice demonstrated hypertrophy, interstitial fibrosis (1.9-fold increase; These translational findings demonstrate a plausible role for endo-MT in HFpEF with cardiorenal syndrome and may have therapeutic implications in drug development for patients with HFpEF and concomitant renal dysfunction.

Sections du résumé

BACKGROUND
The management of clinical heart failure with a preserved ejection fraction (HFpEF) is often complicated by concurrent renal dysfunction, known as the cardiorenal syndrome. This, combined with the notable lack of evidence-based therapies for HFpEF, highlights the importance of examining mechanisms and targetable pathways in HFpEF with the cardiorenal syndrome.
METHODS
HFpEF was induced in mice by uninephrectomy, infusion of
RESULTS
Kidneys from HFpEF mice demonstrated hypertrophy, interstitial fibrosis (1.9-fold increase;
CONCLUSIONS
These translational findings demonstrate a plausible role for endo-MT in HFpEF with cardiorenal syndrome and may have therapeutic implications in drug development for patients with HFpEF and concomitant renal dysfunction.

Identifiants

pubmed: 34407636
doi: 10.1161/CIRCHEARTFAILURE.121.008372
pmc: PMC8575120
mid: NIHMS1728876
doi:

Substances chimiques

Biomarkers 0
Aldosterone 4964P6T9RB

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

e008372

Subventions

Organisme : NHLBI NIH HHS
ID : R01 HL145985
Pays : United States
Organisme : NHLBI NIH HHS
ID : T32 HL007224
Pays : United States
Organisme : NHLBI NIH HHS
ID : T32 HL125232
Pays : United States

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Auteurs

María Valero-Muñoz (M)

Department of Medicine, Whitaker Cardiovascular Institute (M.V.-M., A.O., E.F., R.B.-R., F.S.), Boston University School of Medicine, MA.

Albin Oh (A)

Department of Medicine, Whitaker Cardiovascular Institute (M.V.-M., A.O., E.F., R.B.-R., F.S.), Boston University School of Medicine, MA.

Elizabeth Faudoa (E)

Department of Medicine, Whitaker Cardiovascular Institute (M.V.-M., A.O., E.F., R.B.-R., F.S.), Boston University School of Medicine, MA.

Rosa Bretón-Romero (R)

Department of Medicine, Whitaker Cardiovascular Institute (M.V.-M., A.O., E.F., R.B.-R., F.S.), Boston University School of Medicine, MA.

Fatima El Adili (F)

Department of Rheumatology, Arthritis and Autoimmune Diseases Research Center (F.E.A., A.B.), Boston University School of Medicine, MA.

Andreea Bujor (A)

Department of Rheumatology, Arthritis and Autoimmune Diseases Research Center (F.E.A., A.B.), Boston University School of Medicine, MA.

Flora Sam (F)

Department of Medicine, Whitaker Cardiovascular Institute (M.V.-M., A.O., E.F., R.B.-R., F.S.), Boston University School of Medicine, MA.

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