Arq. Bras. Cardiol. 2024; 121(10): e20240698
Long Non-Coding RNA CCAT2 and Pathological Cardiac Remodeling
Gustavo Augusto Ferreira Mota
, Mariana Gatto
, Claudia Maria Silva Cyrino, Silvio Assis de Oliveira Júnior, Marina Politi Okoshi
This Short Editorial is referred by the Research article "LncRNA CCAT2 Knockdown Alleviates Pressure Overload or Ang II-Induced Cardiac Hypertrophy Via Disruption of the Wnt/β-Catenin Signaling".
Despite advances in cardiovascular medicine, heart disease is a serious public health problem due to its high prevalence, elevated cost, and high morbidity and mortality. Therefore, it is necessary to improve the understanding of molecular mechanisms involved in the pathophysiology of cardiovascular disease.
Following cardiac injury, the heart undergoes a remodeling process, initially characterized by alterations in the genome expression. The changes lead to molecular, cellular, and interstitial modifications that manifest clinically as variations in the size, shape, and function of the heart. Cardiac remodeling is usually accompanied by activation of neurohormonal systems. Under physiological conditions, the renin-angiotensin system plays a fundamental role in regulating blood pressure and fluid-electrolyte balance. However, when excessively activated, it induces deleterious effects on the heart, such as myocyte hypertrophy and death and interstitial myocardial fibrosis.
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