Advances in Heart Failure Pharmacotherapy

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Drug Discovery, Development and Delivery".

Deadline for manuscript submissions: 31 July 2026 | Viewed by 702

Editor


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Guest Editor
Department of Basic and Clinical Sciences, University of Nicosia Medical School, 2417 Nicosia, Cyprus
Interests: heart failure; pharmacology; calcium cycling

Special Issue Information

Dear Colleagues,

Heart failure is the final common pathway for many cardiovascular risk factors and diseases. It is a complex clinical syndrome caused by structural or functional abnormalities that impair ventricular filling or ejection, in turn leading to an inability to meet metabolic demands. Despite advances in care, heart failure remains associated with high morbidity and mortality. An estimated 26 million people live with chronic heart failure worldwide, with substantial healthcare costs and marked reduction in quality of life. Guideline-directed medical therapy emphasizes the modulation of overactive neurohormonal pathways, using a quadruple regimen that includes β-blockers, renin angiotensin aldosterone system inhibitors or angiotensin receptor neprilysin inhibitors, mineralocorticoid receptor antagonists, and sodium glucose cotransporter 2 inhibitors. Treatment response varies widely between individuals, and the optimal regimen for a given patient may differ based on individual factors, such as sex, disease phenotype, complications, and co-morbidities.

This Special Issue focuses on advancing pharmacotherapy for heart failure, including studies focusing on personalized medicine. We welcome clinical and pre-clinical mechanistic studies, as well as rigorous evidence syntheses, that evaluate novel therapeutic targets, combinations, and treatment algorithms. Submissions that address variations in pharmacokinetics and pharmacodynamics, sequencing or dosing protocols, biomarker or genotype-guided care, and drug combinations that reduce adverse clinical outcomes while providing mechanistic insight are also encouraged.

Dr. Persoulla A. Nicolaou
Guest Editor

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Keywords

  • heart failure
  • pharmacotherapy
  • precision medicine
  • pharmacogenomics
  • pharmacokinetics
  • pharmacodynamics

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Published Papers (1 paper)

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Review

26 pages, 3554 KB  
Review
AMPK Signalling in Heart Failure: From Metabolic Sensor to Context-Dependent Therapeutic Target
by Rayan Arzouni, Reem Aazar, Seif Asakrieh, Seif Cattan and Aleksandar Jovanović
Biomedicines 2026, 14(6), 1362; https://doi.org/10.3390/biomedicines14061362 - 17 Jun 2026
Viewed by 350
Abstract
Heart failure (HF) is a complex clinical syndrome characterized not only by impaired cardiac function but also by profound disturbances in myocardial energy metabolism. AMP-activated protein kinase (AMPK), a central cellular energy sensor, plays a critical role in maintaining metabolic homeostasis by coordinating [...] Read more.
Heart failure (HF) is a complex clinical syndrome characterized not only by impaired cardiac function but also by profound disturbances in myocardial energy metabolism. AMP-activated protein kinase (AMPK), a central cellular energy sensor, plays a critical role in maintaining metabolic homeostasis by coordinating pathways involved in substrate utilization, mitochondrial function, autophagy, and stress adaptation. Experimental evidence supports a cardioprotective role of AMPK activation, including improved energetic efficiency, attenuation of pathological remodeling, and enhanced cellular resilience. However, emerging data indicate that AMPK signaling is highly context-dependent, with its effects varying according to HF phenotype, disease stage, and isoform-specific activity. While indirect AMPK modulation through established therapies such as metformin and sodium-glucose cotransporter 2 (SGLT2) inhibitors has demonstrated clinical benefit, the specific contribution of AMPK to these effects remains incompletely defined. Furthermore, direct pharmacological activation is limited by challenges including tissue specificity, off-target effects, and potential adverse outcomes associated with sustained activation. This review provides a comprehensive overview of AMPK signaling in HF, focusing on its role in metabolic remodeling, mitochondrial regulation, and interaction with key cardioprotective pathways. We also examine current clinical and translational evidence and discuss emerging strategies aimed at achieving isoform-selective and tissue-specific modulation. Collectively, these insights support a shift from broad AMPK activation toward precision-based therapeutic approaches tailored to the disease context. Full article
(This article belongs to the Special Issue Advances in Heart Failure Pharmacotherapy)
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