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Pharmacological Approaches in Inflammation, Aging, and Cardiovascular Diseases

A Special Issue of International Journal of Molecular Sciences (ISSN 1422-0067) belonging to the section "Molecular Pharmacology".

Deadline for manuscript submissions: 20 October 2026 | Viewed by 2476

Editors


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Guest Editor
Department of Cardiac Surgery, University Hospital Zurich, 8091 Zurich, Switzerland
Interests: minimally invasive cardiac surgery; reconstructive surgery; heart failure; cardiopulmonary bypass; aortic diseases; heart valve diseases; mitral valve surgery; coronary artery bypass surgery; off-pump coronary artery bypass; TAVI; thoracic aortic aneurysm; thoracic aorta; hemodynamics perfusion; aortic valve; coronary artery bypass
Special Issues, Collections and Topics in MDPI journals
Faculty of Medicine, University of Zürich, 8032 Zurich, Switzerland
Interests: pharmacological strategy; hypertension; myocardial infarction; cardiovascular disorders

Special Issue Information

Dear Colleagues,

Inflammation and aging are key drivers of cardiovascular disease (CVD) progression. Advances in molecular biology, bioinformatics, and translational research have paved the way to extensive research on the underlying mechanisms, opening potential avenues for targeted therapeutic strategies. At the same time, cardiac surgery remains an essential component in the management of advanced CVD, yet it is associated with inflammatory responses that can significantly affect patient outcomes.

We are pleased to invite you to contribute to this Special Issue, which focuses on innovative pharmacological approaches to understanding and addressing inflammation, aging, and CVD, integrating insights from bench to bedside.

This Special Issue aims to provide a comprehensive and state-of-the-art overview of this critical area, highlighting the multifaceted roles of inflammation and aging in cardiovascular diseases.

In this Issue, original research articles, reviews, commentaries, and meta-analyses are welcome. Research areas may include (but are not limited to) the following:

  • Mechanisms linking inflammation, aging, and cardiovascular disease;
  • Biomarkers and diagnostic tools;
  • Translational and bioinformatics approaches;
  • Inflammation and outcomes in cardiac surgery;
  • Cardiometabolic health and vascular aging;
  • Therapeutic/pharmacological strategies and interventions.

We look forward to receiving your contributions.

Prof. Dr. Omer Dzemali
Dr. Era Gorica
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized 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

  • inflammation
  • aging
  • cardiovascular diseases
  • approaches
  • translational research
  • therapeutic targets

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Published Papers (3 papers)

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Research

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19 pages, 21412 KB  
Article
Calycosin Attenuates LPS-Induced Cardiomyocyte Injury Through Regulation of the PPARγ/NF-κB Signaling Pathway
by Rui Zhao, Zhiwang Wang, Wuzhou Liu and Keke Liang
Int. J. Mol. Sci. 2026, 27(19), 8505; https://doi.org/10.3390/ijms27198505 - 23 Sep 2026
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Abstract
Calycosin (CAL) is an isoflavone monomer derived from Astragalus membranaceus that possesses potent anti-inflammatory and antioxidative pharmacological activities. However, the specific role of CAL in lipopolysaccharide (LPS)-induced inflammatory injury in cardiomyocytes remains to be elucidated. In this study, we established an in vitro [...] Read more.
Calycosin (CAL) is an isoflavone monomer derived from Astragalus membranaceus that possesses potent anti-inflammatory and antioxidative pharmacological activities. However, the specific role of CAL in lipopolysaccharide (LPS)-induced inflammatory injury in cardiomyocytes remains to be elucidated. In this study, we established an in vitro inflammatory injury model using LPS-stimulated H9c2 cardiomyocytes to evaluate the cardioprotective effects of CAL. We assessed cell viability, live/dead cell staining, oxidative stress markers, inflammatory cytokine profiles, and cardiac injury biomarkers to characterize the protective efficacy of CAL. Quantitative proteomics combined with bioinformatics analysis was employed to explore the underlying mechanisms. Molecular docking and molecular dynamics simulations were performed to analyze the predicted binding affinity and complex stability between CAL and the target proteins PPARγ and NF-κB. PPARγ and NF-κB mRNA and protein levels were measured by qPCR and Western blotting, and rescue experiments with the PPARγ-specific inhibitor GW9662 were performed to validate target dependency. Our results demonstrated that CAL exerted significant protective effects against LPS-induced cardiomyocyte injury, effectively enhancing cell viability, reducing cell death, alleviating intracellular ROS accumulation, modulating oxidative stress-related parameters, suppressing excessive inflammatory responses, and decreasing the release of cardiac injury biomarkers. Proteomic analysis revealed that differentially expressed proteins were significantly enriched in the PPAR signaling pathway. Molecular simulations predicted that CAL binds stably to both PPARγ and NF-κB. PCR and Western blotting results showed that CAL upregulated PPARγ and suppressed NF-κB-mediated pro-inflammatory gene expression at both the mRNA and protein levels. Notably, pharmacological blockade of PPARγ with GW9662 partially abolished the cardioprotective effects of CAL. Collectively, these findings indicate that CAL ameliorates LPS-induced inflammatory injury in H9c2 cardiomyocytes through a protective mechanism that depends on activation of PPARγ and subsequent inhibition of the NF-κB signaling pathway. Full article
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Review

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16 pages, 1248 KB  
Review
The Gut–Heart Axis in Cardiovascular Disease: Microbial Metabolites, Mediterranean and Traditional Turkish Dietary Patterns, and Personalized Medicine
by Melih Erol Ceyhan, Gentiana Mehmeti, Sude Nazli Cukurova and Şeyma Dümür
Int. J. Mol. Sci. 2026, 27(18), 8311; https://doi.org/10.3390/ijms27188311 (registering DOI) - 18 Sep 2026
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Abstract
Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality globally. Increasing evidence identifies the gut microbiota as one of the major regulators of cardiovascular health, leading to the concept of the gut–heart axis. Metabolites from microbiota serve as key mediators linking [...] Read more.
Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality globally. Increasing evidence identifies the gut microbiota as one of the major regulators of cardiovascular health, leading to the concept of the gut–heart axis. Metabolites from microbiota serve as key mediators linking intestinal microbial activity with vascular and metabolic processes. This comprehensive narrative review was conducted using PubMed and Scopus databases, focusing on studies published between 2015 and 2025, along with selected seminal studies, to show the role of gut microbiota and its metabolites in CVD. Microbial metabolites exert various important and often opposing effects on cardiovascular physiology. Trimethylamine N-oxide (TMAO), derived from dietary choline and carnitine metabolism, promotes atherosclerosis through endothelial dysfunction, inflammation, foam cell formation, impaired cholesterol transport, and enhanced platelet reactivity. In contrast, short-chain fatty acids (SCFAs), produced by microbial fermentation of dietary fibers, exert protective effects by reducing inflammation, improving endothelial function, and maintaining intestinal barrier integrity by G protein coupled receptor activation and histone deacetylase inhibition. Disruption of gut barrier function facilitates lipopolysaccharide translocation, contributing to systemic inflammation and cardiometabolic risk. Bile acids further modulate cardiovascular processes through FXR and TGR5 signaling pathways; this influences lipid metabolism and inflammatory responses. Dietary patterns, including the Mediterranean diet and dietary diversity in Türkiye, play a central role in shaping microbiota composition and metabolite balance. The gut–heart axis represents a complex and dynamic process in which microbiota-derived metabolites exert a critical influence on cardiovascular health and disease. Modulation of the gut microbiome through dietary interventions, microbiota-targeted therapies, and emerging personalized strategies offers promising avenues for the prevention and management of CVDs. Future research should focus on microbiome-based precision approaches and large-scale clinical validation to facilitate translation into clinical practice. Full article
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17 pages, 281 KB  
Review
Topical Probiotics in Diabetic Wound Healing: Emerging Therapeutic Strategies
by Eni Çelo, Aida Dama, Sokol Hasho and Leonard Deda
Int. J. Mol. Sci. 2026, 27(6), 2826; https://doi.org/10.3390/ijms27062826 - 20 Mar 2026
Cited by 4 | Viewed by 1630
Abstract
Diabetic foot ulcers (DFUs) are among the most serious and costly complications of diabetes, characterised by delayed healing, frequent infections, and a high risk of recurrence. Despite advances in wound care, many current therapies fail to address the multifactorial pathophysiology of diabetic wounds, [...] Read more.
Diabetic foot ulcers (DFUs) are among the most serious and costly complications of diabetes, characterised by delayed healing, frequent infections, and a high risk of recurrence. Despite advances in wound care, many current therapies fail to address the multifactorial pathophysiology of diabetic wounds, including vascular dysfunction, immune dysregulation, chronic inflammation, and microbial imbalance. In this context, topical probiotics have emerged as a promising microbiome-based strategy aimed at restoring microbial balance while promoting tissue repair. This review summarises current evidence on the use of topical probiotics in diabetic wound healing, with a particular focus on DFUs, outlining key pathophysiological barriers to healing and examining how probiotic therapies may counteract these processes through antimicrobial, antibiofilm, immunomodulatory, and pro-angiogenic mechanisms. Preclinical studies suggest that topical probiotics may promote accelerated wound closure, reduce bacterial burden, modulate inflammatory responses, and enhance collagen deposition and angiogenesis following topical probiotic application. Early clinical studies investigations remain limited to small pilot studies and case series but have reported preliminary signals of enhanced healing and acceptable short-term tolerability in small exploratory cohorts. In addition, recent advances in probiotic delivery, such as bioengineered dressings, postbiotic formulations, and nano-enabled systems designed to improve stability and therapeutic performance, are also discussed. While existing data indicate biological plausibility and early clinical feasibility, larger, well-designed randomized controlled trials and deeper mechanistic investigations are still required to confirm efficacy, clarify safety in high-risk populations, and enable responsible clinical translation. Full article
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