Targeting Collagen Pathways as an HFpEF Therapeutic Strategy

Alice Bonanni, Ramona Vinci, Alessia D'Aiello, Maria Chiara Grimaldi, Marianna Di Sario, Dalila Tarquini, Luca Proto, Anna Severino, Daniela Pedicino, Giovanna Liuzzo

Research output: Contribution to journalArticle

Abstract

Heart failure with preserved ejection fraction (HFpEF) is a complex and heterogeneous clinical syndrome. The prevalence is expected to increase in the coming years, resulting in heart failure with reduced ejection fraction (HFrEF). This condition poses a burden to the global health care system as the number of patients affected by this condition is constantly increasing due to a rising average lifespan. The absence of validated drugs effective in reducing hospitalization rates and mortality may reflect the impossibility of applying a one size fits all approach as in HFrEF, heading for a personalized approach. Available evidence demonstrated the link between collagen quantity and quality alterations, and cardiac remodeling. In the context of fibrosis, collagen cross-linking is strictly involved, displaying two types of mechanisms: enzymatic and non-enzymatic. In the murine model, enzymatic inhibition of fibrosis-inducing protease-activated receptor-1 (PAR1) and transforming growth factor (TGF)-& beta; signaling appeared to reduce cardiac fibrosis. On the other hand, in the case of non-enzymatic cross-linking, sodium glucose co-transporter type 2 inhibitors (SGLT2is), appeared to counteract the deposition of advanced glycation end-products (AGEs), which in turn contributed to ventricular remodeling. In this review, we address the mechanisms associated with collagen alterations to identify potential targets of cardiac fibrosis in HFpEF patients.
Original languageEnglish
Pages (from-to)N/A-N/A
JournalJournal of Clinical Medicine
Volume12
DOIs
Publication statusPublished - 2023

Keywords

  • AGEs
  • HFpEF
  • SGLT2i
  • cardiac remodeling
  • collagen
  • coronary microvascular dysfunction

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