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Molecular Mechanisms and Therapeutic Targets in Cardiometabolic Disorders
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Molecular Mechanisms and Therapeutic Targets in Cardiometabolic Disorders

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 20 February 2026 | Viewed by 894

Special Issue Editors

Prof. Dr. Massimiliano M. Corsi Romanelli

E-Mail Website
Guest Editor
Department of Biomedical Sciences for Health, University of Milan, 00133 Milan, Italy
Interests: cardiometabolic disorders
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Pietro Formisano

E-Mail Website
Guest Editor
Department of Translational Medical Sciences, University of Naples Federico II, 80131 Naples, Italy
Interests: adipose tissue; growth factors; inflammation; insulin resistance; tumor–microenvironment interaction; tissue regeneration
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular disease (CVD) is a global challenge in modern society. Significant progress has been made in the pathophysiology of atherosclerotic lesion formation and complications such as myocardial infarction, stroke, and peripheral vascular disease. Yet, despite these advances, therapeutic options that can significantly reduce morbidity and mortality remain limited, indicating that the mechanism of atherosclerosis needs further elucidation. Therefore, understanding the molecular mechanisms and discovering novel therapeutic targets for atherosclerosis are urgently needed for the development of effective treatments for heart diseases.
Understanding the mechanisms involved in the development of atherosclerosis is challenging due to the complexity of today’s picture of the pathogenesis of atherosclerosis.
The molecular factors of atherosclerosis including renin–angiotensin signaling, vascular endothelial injury, lipid accumulation, smooth muscle cell phenotypic transition, macrophage infiltration, and inflammation alone or in combination contribute to the onset and progress of the atherosclerotic injuries and obesity. Metabolic dysfunctions with the clustering of risk factors are key factors that greatly worsen the atherosclerotic processes. In this Special Issue, we encourage submissions that identify the possible mechanisms for the prevention of progression of atherosclerosis. Clinical research for the early diagnosis and prognosis of cardiometabolic obesity-related diseases will also be welcomed.
We welcome submissions focusing on but not limited to topics mentioned below:

  1. Role of vascular endothelial injury in the development of atherosclerosis.
  2. Regulation of the inflammatory response in atherosclerosis.
  3. Novel molecular factors as potential targets in atherosclerosis treatment.
  4. Clinical research on novel biomarkers for the early diagnosis and prognosis of cardiac diseases.
  5. Obesity and other dysmetabolic conditions and cardiovascular diseases: biomarkers and new drugs.

Prof. Dr. Massimiliano M. Corsi Romanelli
Prof. Dr. Pietro Formisano
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • atherosclerosis
  • angiotensin
  • endothelial cell
  • inflammation
  • biomarkers
  • gLP-1
  • sT-2

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Published Papers (1 paper)

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Research

21 pages, 3852 KiB  
Article
PCSK9 Inhibitor Inclisiran Attenuates Cardiotoxicity Induced by Sequential Anthracycline and Trastuzumab Exposure via NLRP3 and MyD88 Pathway Inhibition
by Vincenzo Quagliariello, Massimiliano Berretta, Irma Bisceglia, Martina Iovine, Matteo Barbato, Raffaele Arianna, Maria Laura Canale, Andrea Paccone, Alessandro Inno, Marino Scherillo, Stefano Oliva, Christian Cadeddu Dessalvi, Alfredo Mauriello, Carlo Maurea, Celeste Fonderico, Anna Chiara Maratea, Domenico Gabrielli and Nicola Maurea
Int. J. Mol. Sci. 2025, 26(14), 6617; https://doi.org/10.3390/ijms26146617 - 10 Jul 2025
Viewed by 264
Abstract
Cardiotoxicity related to anthracyclines and trastuzumab represents a significant clinical challenge in cancer therapy, often limiting treatment efficacy and patient survival. The underlying mechanisms of cardiotoxicity involve the activation of NLRP3 and the MyD88-dependent signaling pathway. Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i), [...] Read more.
Cardiotoxicity related to anthracyclines and trastuzumab represents a significant clinical challenge in cancer therapy, often limiting treatment efficacy and patient survival. The underlying mechanisms of cardiotoxicity involve the activation of NLRP3 and the MyD88-dependent signaling pathway. Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i), such as inclisiran, are known for their lipid-lowering effects, but emerging data indicate that they may also exert pleiotropic benefits beyond cholesterol reduction. This study investigates whether inclisiran can mitigate the cardiotoxic effects of anthracyclines and trastuzumab through reduction of NLRP3 activation and MyD88 signaling, independently of its effects on dyslipidemia. Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) were exposed to subclinical concentrations of doxorubicin (1 µM) and trastuzumab in sequential therapy (200 nM), alone or in combination with inclisiran (100 nM) for 24 h. After the incubation period, we performed the following tests: determination of cardiomyocytes apoptosis, analysis of intracellular reactive oxygen species, lipid peroxidation products (including malondialdehyde and 4-hydroxynonenal), intracellular mitofusin-2 and Ca++ levels. Troponin and BNP were quantified through selective ELISA methods. A confocal laser scanning microscope was used to study cardiomyocyte morphology and F-actin staining after treatments. Moreover, pro-inflammatory studies were also performed, including the intracellular expression of NLRP-3, MyD-88 and twelve cytokines/growth factors involved in cardiotoxicity (IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-10, IL-12, IL17-α, IFN-γ, TNF-α, G-CSF, GM-CSF). Inclisiran co-incubated with doxorubicin and trastuzumab exerts significant cardioprotective effects, enhancing cell viability by 88.9% compared to only DOXO/TRA treated cells (p < 0.001 for all). Significant reduction of oxidative stress, and intracellular levels of NLRP-3, MyD88, IL-1α, IL-1β, IL-6, IL-12, IL17-α, TNF-α, G-CSF were seen in the inclisiran group vs. only DOXO/TRA (p < 0.001). For the first time, PCSK9i inclisiran has been shown to exert significant anti-inflammatory effects to reduce anthracycline-HER-2 blocking agent-mediated cardiotoxicity through NLRP-3 and Myd-88 related pathways. The overall conclusions of the study warrant further investigation of the use of PCSK9i in primary prevention of CTRCD in cancer patients, independently from dyslipidemia. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targets in Cardiometabolic Disorders)
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