Cardiac Remodelling Part 1: From Cells and Tissues to Circulating Biomarkers.
Fiche publication
Date publication
mars 2022
Journal
European journal of heart failure
Auteurs
Membres identifiés du Cancéropôle Est :
Pr ROSSIGNOL Patrick
Tous les auteurs :
González A, Richards AM, de Boer RA, Thum T, Arfsten H, Hülsmann M, Falcao-Pires I, Díez J, Foo RS, Chan MYY, Aimo A, Anene-Nzelu GC, Abdelhamid M, Adamopoulos S, Anker SD, Belenkov Y, Gal TB, Cohen-Solal A, Böhm M, Chioncel O, Delgado V, Emdin M, Jankowska EA, Gustafsson F, Hill L, Jaarsma T, Januzzi JL, Jhund PS, Lopatin Y, Lund LH, Metra M, Milicic D, Moura B, Mueller C, Mullens W, Núñez J, Piepoli MF, Rakisheva A, Ristic A, Rossignol P, Savarese G, Tocchetti CG, Van Linthout S, Volterrani M, Seferovic P, Rosano G, Coats AJ, Bayes-Genis A
Lien Pubmed
Résumé
Cardiac remodelling refers to changes in left ventricular (LV) structure and function over time, with a progressive deterioration that may lead to heart failure (HF) development (adverse remodelling) or vice versa a recovery in response to HF treatment. Adverse remodelling predicts a worse outcome, whilst reverse remodelling predicts a better prognosis. The geometry, systolic and diastolic function and electric activity of the left ventricle are affected, as well as the left atrium and on the long term even right heart chambers. At a cellular and molecular level, remodelling involves all components of cardiac tissue: cardiomyocytes, fibroblasts, endothelial cells and leukocytes. The molecular, cellular and histological signatures of remodelling may differ according to the cause and severity of cardiac damage, and clearly to the global trend toward worsening or recovery. These processes cannot be routinely evaluated through endomyocardial biopsies, but may be reflected by circulating levels of several biomarkers. Different classes of biomarkers (e.g., proteins, non-coding RNAs, metabolites and/or epigenetic modifications) and many biomarkers of each class might inform on some aspects on HF development, progression and long-term outcomes, but most have failed to enter clinical practice. This may be due to the biological complexity of remodelling, so that no single biomarker could provide great insight on remodelling when assessed alone. Another possible reason is a still incomplete understanding of the role of biomarkers in the pathophysiology of cardiac remodelling. Such role will be investigated in the first part of review paper on biomarkers of cardiac remodelling. This article is protected by copyright. All rights reserved.
Référence
Eur J Heart Fail. 2022 Mar 25;: