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Special Issue "Aging and Heart Disease"

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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: closed (15 June 2023) | Viewed by 10924

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Special Issue Editors

Prof. Dr. Giuseppe Rengo

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Guest Editor

Department of Translational Medical Sciences, University of Naples Federico II, Naples, Italy
Interests: heart failure; sympathetic nervous system; ageing; beta-adrenergic receptors; biomarkers; cardiac remodeling; frailty
Special Issues, Collections and Topics in MDPI journals

Dr. Claudio de Lucia

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Guest Editor

Istituti Clinici Scientifici Maugeri SpA Società Benefit (ICS Maugeri SpA SB), Scientific Institute of Telese Terme, Telese Terme (BN), Italy
Interests: aging; geriatrics; cardiovascular diseases, heart failure; myocardial infarction; sympathetic nervous system

Dr. Leonardo Bencivenga

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Guest Editor

1. Gérontopôle de Toulouse, Institut du Vieillissement, CHU de Toulouse, France
2. Department of Advanced Biomedical Sciences, University of Naples “Federico II”, Naples, Italy
Interests: aging; frailty; geriatric syndromes; heart failure; sympathetic nervous system; hallmarks of aging; biomarkers; cardiac remodeling; hypertension

Special Issue Information

Dear Colleagues,

The global population is aging at a faster rate than expected. Improvements in the prevention, diagnosis, and treatment of cardiovascular diseases have been outstanding in the last few decades, thus concurring to the higher prevalence of heart diseases in people aged ≥65, which often also suffer from frailty and disability. The burden of cardiovascular disease affects the structure, function, and metabolism of the heart and manifests with multiple conditions, such as coronary artery disease, myocardial infarction, arrhythmias, and heart failure. Aging and cardiovascular disease share several common pathophysiological features, involving inflammatory, metabolic, and several other pathways which concur, in the long term, to the loss of intrinsic capacity among the elderly, leading to dependence in daily life activities and reduced quality of life for caregivers too.

Potential topics include, but are not limited to: new therapeutic approaches to prevent, reduce, or reverse cardiac aging; circulating biomarkers of cardiac dysfunction and failure during aging; the role of epigenetics, inflammation, and immune system in the establishment and development of age-related cardiac dysfunction; and HFpEF.

For this Special Issue, we invite investigators to contribute with original research and review papers. Preclinical, translational, and clinical studies which emphasise molecular biology approaches are of interest.

Prof. Dr. Giuseppe Rengo
Dr. Claudio de Lucia
Dr. Leonardo Bencivenga
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

heart disease
aging
geriatrics
frailty
signaling pathways

Published Papers (6 papers)

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Research

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Open AccessArticle

Aging Model for Analyzing Drug-Induced Proarrhythmia Risks Using Cardiomyocytes Differentiated from Progeria-Patient-Derived Induced Pluripotent Stem Cells

Neil Daily

Julian Elson

and

Tetsuro Wakatsuki

Int. J. Mol. Sci. 2023, 24(15), 11959; https://doi.org/10.3390/ijms241511959 - 26 Jul 2023

Viewed by 369

Abstract

Among various cardiac safety concerns, proarrhythmia risks, including QT prolongation leading to Torsade de Pointes, is one of major cause for drugs being withdrawn (~45% 1975–2007). Preclinical study requires the evaluation of proarrhythmia using in silico, in vitro, and/or animal models. Considering that the primary consumers of prescription drugs are elderly patients, applications of “aging-in-a-dish” models would be appropriate for screening proarrhythmia risks. However, acquiring such models, including cardiomyocytes (CMs) derived from induced pluripotent stem cells (iPSCs), presents extensive challenges. We proposed the hypothesis that CMs differentiated from iPSCs derived from Hutchinson–Gilford progeria syndrome (HGPS, progeria) patients, an ultra-rare premature aging syndrome, can mimic the phenotypes of aging CMs. Our objective, therefore, was to examine this hypothesis by analyzing the response of 11 reference compounds utilized by the Food and Drug Administration (FDA)’s Comprehensive in vitro Proarrhythmia Assay (CiPA) using progeria and control CMs. As a sensitive surrogate marker of modulating cardiac excitation–contraction coupling, we evaluated drug-induced changes in calcium transient (CaT). We observed that the 80% CaT peak duration in the progeria CMs (0.98 ± 0.04 s) was significantly longer than that of control CMs (0.70 ± 0.05 s). Furthermore, when the progeria CMs were subjected to four doses of 11 compounds from low-, intermediate-, and high-risk categories, they demonstrated greater arrhythmia susceptibility than control cells, as shown through six-parameter CaT profile analyses. We also employed the regression analysis established by CiPA to classify the 11 reference compounds and compared proarrhythmia susceptibilities between the progeria and control CMs. This analysis revealed a greater proarrhythmia susceptibility in the progeria CMs compared to the control CMs. Interestingly, in both CMs, the compounds categorized as low risk did not exceed the safety risk threshold of 0.8. In conclusion, our study demonstrates increased proarrhythmia sensitivity in progeria CMs when tested with reference compounds. Future studies are needed to analyze underlying mechanisms and further validate our findings using a larger array of reference compounds. Full article

(This article belongs to the Special Issue Aging and Heart Disease)

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Open AccessArticle

Fluoxetine Treatment Decreases Cardiac Vagal Input and Alters the Serotonergic Modulation of the Parasympathetic Outflow in Diabetic Rats

Mónica García-Domingo

José Ángel García-Pedraza

Juan Francisco Fernández-González

Cristina López

María Luisa Martín

and

Asunción Morán

Int. J. Mol. Sci. 2022, 23(10), 5736; https://doi.org/10.3390/ijms23105736 - 20 May 2022

Cited by 1 | Viewed by 1191

Abstract

Comorbid diabetes and depression constitutes a major health problem, worsening associated cardiovascular diseases. Fluoxetine’s (antidepressant) role on cardiac diabetic complications remains unknown. We determined whether fluoxetine modifies cardiac vagal input and its serotonergic modulation in male Wistar diabetic rats. Diabetes was induced by alloxan and maintained for 28 days. Fluoxetine was administered the last 14 days (10 mg/kg/day; p.o). Bradycardia was obtained by vagal stimulation (3, 6 and 9 Hz) or i.v. acetylcholine administrations (1, 5 and 10 μg/kg). Fluoxetine treatment diminished vagally-induced bradycardia. Administration of 5-HT originated a dual action on the bradycardia, augmenting it at low doses and diminishing it at high doses, reproduced by 5-CT (5-HT_1/7 agonist). 5-CT did not alter the bradycardia induced by exogenous acetylcholine. Decrease of the vagally-induced bradycardia evoked by high doses of 5-HT and 5-CT was reproduced by L-694,247 (5-HT_1D agonist) and blocked by prior administration of LY310762 (5-HT_1D antagonist). Enhancement of the electrical-induced bradycardia by 5-CT (10 μg/kg) was abolished by pretreatment with SB269970 (5-HT₇ receptor antagonist). Thus, oral fluoxetine treatment originates a decrease in cardiac cholinergic activity and changes 5-HT modulation of bradycardic responses in diabetes: prejunctional 5-HT₇ receptors augment cholinergic-evoked bradycardic responses, whereas prejunctional 5-HT_1D receptors inhibit vagally-induced bradycardia. Full article

(This article belongs to the Special Issue Aging and Heart Disease)

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Review

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Open AccessReview

Aging of the Arterial System

and

Alessandro P. Delitala

Int. J. Mol. Sci. 2023, 24(8), 6910; https://doi.org/10.3390/ijms24086910 - 07 Apr 2023

Cited by 3 | Viewed by 1107

Abstract

Aging of the vascular system is associated with deep changes of the structural proprieties of the arterial wall. Arterial hypertension, diabetes mellitus, and chronic kidney disease are the major determinants for the loss of elasticity and reduced compliance of vascular wall. Arterial stiffness is a key parameter for assessing the elasticity of the arterial wall and can be easily evaluated with non-invasive methods, such as pulse wave velocity. Early assessment of vessel stiffness is critical because its alteration can precede clinical manifestation of cardiovascular disease. Although there is no specific pharmacological target for arterial stiffness, the treatment of its risk factors helps to improve the elasticity of the arterial wall. Full article

(This article belongs to the Special Issue Aging and Heart Disease)

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Open AccessReview

Inflammageing and Cardiovascular System: Focus on Cardiokines and Cardiac-Specific Biomarkers

Marco Alfonso Perrone

Alberto Aimo

Sergio Bernardini

and

Aldo Clerico

Int. J. Mol. Sci. 2023, 24(1), 844; https://doi.org/10.3390/ijms24010844 - 03 Jan 2023

Cited by 6 | Viewed by 1734

Abstract

The term “inflammageing” was introduced in 2000, with the aim of describing the chronic inflammatory state typical of elderly individuals, which is characterized by a combination of elevated levels of inflammatory biomarkers, a high burden of comorbidities, an elevated risk of disability, frailty, and premature death. Inflammageing is a hallmark of various cardiovascular diseases, including atherosclerosis, hypertension, and rapid progression to heart failure. The great experimental and clinical evidence accumulated in recent years has clearly demonstrated that early detection and counteraction of inflammageing is a promising strategy not only to prevent cardiovascular disease, but also to slow down the progressive decline of health that occurs with ageing. It is conceivable that beneficial effects of counteracting inflammageing should be most effective if implemented in the early stages, when the compensatory capacity of the organism is not completely exhausted. Early interventions and treatments require early diagnosis using reliable and cost-effective biomarkers. Indeed, recent clinical studies have demonstrated that cardiac-specific biomarkers (i.e., cardiac natriuretic peptides and cardiac troponins) are able to identify, even in the general population, the individuals at highest risk of progression to heart failure. However, further clinical studies are needed to better understand the usefulness and cost/benefit ratio of cardiac-specific biomarkers as potential targets in preventive and therapeutic strategies for early detection and counteraction of inflammageing mechanisms and in this way slowing the progressive decline of health that occurs with ageing. Full article

(This article belongs to the Special Issue Aging and Heart Disease)

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Open AccessReview

The Aging Heart: A Molecular and Clinical Challenge

and

Int. J. Mol. Sci. 2022, 23(24), 16033; https://doi.org/10.3390/ijms232416033 - 16 Dec 2022

Cited by 5 | Viewed by 3293

Abstract

Aging is associated with an increasing burden of morbidity, especially for cardiovascular diseases (CVDs). General cardiovascular risk factors, ischemic heart diseases, heart failure, arrhythmias, and cardiomyopathies present a significant prevalence in older people, and are characterized by peculiar clinical manifestations that have distinct features compared with the same conditions in a younger population. Remarkably, the aging heart phenotype in both healthy individuals and patients with CVD reflects modifications at the cellular level. An improvement in the knowledge of the physiological and pathological molecular mechanisms underlying cardiac aging could improve clinical management of older patients and offer new therapeutic targets. Full article

(This article belongs to the Special Issue Aging and Heart Disease)

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Open AccessReview

Heart Failure in Menopause: Treatment and New Approaches

Jaqueline S. da Silva

Tadeu Lima Montagnoli

Mauro Paes Leme de Sá

and

Gisele Zapata-Sudo

Int. J. Mol. Sci. 2022, 23(23), 15140; https://doi.org/10.3390/ijms232315140 - 01 Dec 2022

Cited by 1 | Viewed by 1868

Abstract

Aging is an important risk factor for the development of heart failure (HF) and half of patients with HF have preserved ejection fraction (HFpEF) which is more common in elderly women. In general, sex differences that lead to discrepancies in risk factors and to the development of cardiovascular disease (CVD) have been attributed to the reduced level of circulating estrogen during menopause. Estrogen receptors adaptively modulate fibrotic, apoptotic, inflammatory processes and calcium homeostasis, factors that are directly involved in the HFpEF. Therefore, during menopause, estrogen depletion reduces the cardioprotection. Preclinical menopause models demonstrated that several signaling pathways and organ systems are closely involved in the development of HFpEF, including dysregulation of the renin-angiotensin system (RAS), chronic inflammatory process and alteration in the sympathetic nervous system. Thus, this review explores thealterations observed in the condition of HFpEF induced by menopause and the therapeutic targets with potential to interfere with the disease progress. Full article

(This article belongs to the Special Issue Aging and Heart Disease)

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