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Advances in Heart Diseases: Molecular Pathogenesis, Biomarkers and Therapies
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Advances in Heart Diseases: Molecular Pathogenesis, Biomarkers and Therapies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 May 2025 | Viewed by 2511

Special Issue Editor

Dr. Nadia Aspromonte

E-Mail Website
Guest Editor
Department of Cardiovascular Sciences, Fondazione Policlinico Universitario A. Gemelli, IRCCS, 00168 Rome, Italy
Interests: biomarkers; heart failure; ischemic heart disease; preserved ejection fraction; cardiology; fibrosis; inflammation; non-coding RNA
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In recent decades, significant advancements have been achieved in the diagnosis and management of heart diseases, along with an enhanced understanding of their molecular pathogenesis. These developments have been instrumental in leveraging specific biomarkers to guide increasingly innovative therapeutic interventions. Novel insights into the molecular pathways implicated in disease progression have emerged.

Concurrently, the identification and validation of biomarkers have transformed diagnostic and prognostic approaches, facilitating early detection, streamlined management, and personalized treatment strategies. Biomarkers such as troponins, BNPs, and non-coding RNAs have emerged as invaluable tools in clinical practice, furnishing clinicians with crucial information for patient management. Moreover, therapeutic interventions have undergone substantial evolution, encompassing traditional cardiac pharmacological agents alongside novel pharmacological and interventional therapies, as well as comorbidity treatments, aimed at alleviating disease burden and enhancing patient outcomes.

In this Special Issue, we will explore the strides in molecular understanding, biomarker discovery, and therapeutic innovation, promising a brighter future in the battle against heart disease.

Dr. Nadia Aspromonte
Guest Editor

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

  • heart diseases
  • biomarkers
  • molecular pathways
  • personalized medicine
  • interventional therapies

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Published Papers (2 papers)

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Research

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13 pages, 5113 KiB  
Article
Nlrc4 Inflammasome Expression After Acute Myocardial Infarction in Rats
by Patricia Aparecida Borim, Mariana Gatto, Gustavo Augusto Ferreira Mota, Ana Luiza Barioni Meirelles, Anna Clara Consorti dos Santos, Luana Urbano Pagan, Elida Paula Benquique Ojopi, Eder Anderson Rodrigues, Lidiane Moreira Souza, Felipe Cesar Damatto, Leiliane Rodrigues dos Santos Oliveira, Leonardo Antonio Mamede Zornoff, Katashi Okoshi and Marina Politi Okoshi
Int. J. Mol. Sci. 2025, 26(8), 3697; https://doi.org/10.3390/ijms26083697 - 14 Apr 2025
Viewed by 49
Abstract
Acute myocardial necrosis activates the immune response and inflammatory processes. Although the initial response is helpful in restoring tissue injury, dysregulated and exacerbated inflammation contributes to the progression of cardiac remodeling. Inflammasomes play important roles in post-infarction inflammation. NALP1/NLRP1, NLRP 3, and NLRC4 [...] Read more.
Acute myocardial necrosis activates the immune response and inflammatory processes. Although the initial response is helpful in restoring tissue injury, dysregulated and exacerbated inflammation contributes to the progression of cardiac remodeling. Inflammasomes play important roles in post-infarction inflammation. NALP1/NLRP1, NLRP 3, and NLRC4 are the best-known inflammasomes. NLRP3, which has received the most study in cardiovascular disease, has been linked to increased IL-1β (IL1B) production and caspase-1 activity, as well as impaired cardiac function. The role of NLRP1 and NLRC4 inflammasomes after acute myocardial infarction (MI) is poorly understood. We evaluated the expression of myocardial inflammasomes and inflammatory markers 72 h after MI in rats. Male Wistar rats were divided into Sham (n = 15) and MI (n = 16) groups. MI was induced by ligating the left anterior descending coronary artery. Infarct size was assessed by histology. Myocardial protein and gene expression was analyzed by Western blot and RT-qPCR, respectively. IL-1β (Il1b) concentrations in serum and heart macerate supernatant were evaluated by ELISA. Statistical analysis was performed using Student’s t test. Rats with an MI size less than 30% of the total left ventricle (LV) area were excluded; infarct size was 46 ± 11% of the total LV area in MI. The interstitial collagen fraction was higher in MI. Nlrc4, caspase-1 (Casp1), and IL-1β (Il1b) protein expressions were higher in MI. Nlrp3, Nlrp1, ASC (Pycard), pro-caspase-1, and pro-IL-1β (Il1b) expressions did not differ between groups. Expression of the Nlrp3 and ASC (Pycard) genes, as well as myocardial and serum IL-1β (Il1b) concentrations, was higher in MI. Acute post-myocardial infarction inflammation is characterized by increased protein expression of Nlrc4, caspase-1, and interleukin-1β; increased gene expression of Nlrp3 and ASC (Pycard); and elevated serum and myocardial concentrations of interleukin-1β in combination with an increased myocardial collagen interstitial fraction. Full article
(This article belongs to the Special Issue Advances in Heart Diseases: Molecular Pathogenesis, Biomarkers and Therapies)
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Review

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15 pages, 940 KiB  
Review
Microvascular Dysfunction across the Spectrum of Heart Failure Pathology: Pathophysiology, Clinical Features and Therapeutic Implications
by Giulia La Vecchia, Isabella Fumarulo, Andrea Caffè, Mario Chiatto, Rocco A. Montone and Nadia Aspromonte
Int. J. Mol. Sci. 2024, 25(14), 7628; https://doi.org/10.3390/ijms25147628 - 11 Jul 2024
Cited by 6 | Viewed by 2078
Abstract
Coronary microvascular dysfunction (CMD) plays a crucial role across the spectrum of heart failure (HF) pathology, contributing to disease development, progression, and outcomes. The pathophysiological mechanisms linking CMD to HF are complex and still not completely understood and include chronic inflammation, oxidative stress, [...] Read more.
Coronary microvascular dysfunction (CMD) plays a crucial role across the spectrum of heart failure (HF) pathology, contributing to disease development, progression, and outcomes. The pathophysiological mechanisms linking CMD to HF are complex and still not completely understood and include chronic inflammation, oxidative stress, and neurohormonal activation. Despite the diagnostic and prognostic relevance in patients with HF, there is no specific therapeutic strategy targeting CMD to date. Moreover, the diagnosis of this clinical condition is challenging. In this review article, we aim to discuss the different clinical pathogenetic mechanisms linking CMD to HF across the different spectra of these diseases, their prognostic relevance, and the possible therapeutic targets along with the remaining knowledge gaps in the field. Full article
(This article belongs to the Special Issue Advances in Heart Diseases: Molecular Pathogenesis, Biomarkers and Therapies)
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