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Cardiovascular Disease: From Molecular Mechanisms to Therapeutic Innovations
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Cardiovascular Disease: From Molecular Mechanisms to Therapeutic Innovations

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 May 2026 | Viewed by 8145

Special Issue Editor

Dr. Andrea Marzullo

E-Mail Website
Guest Editor
Section of Pathology, Department of Precision and Regenerative Medicine and Ionian Area (DIMEPReJ), University of Bari, 70124 Bari, Italy
Interests: cardiovascular pathology; head and neck diseases; immunohistochemistry; autopsies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular disease (CVD) is the leading global cause of death driven by complex genetic, molecular, and environmental factors. Advances in molecular biology have shed light on key pathways, including inflammation, oxidative stress, and lipid metabolism, offering critical insights into the mechanisms underlying conditions such as atherosclerosis and heart failure. However, challenges remain in translating these findings into effective therapies and addressing variability across populations.

This Special Issue focuses on the molecular underpinnings of CVD and their implications for innovative therapeutic strategies. We welcome advanced studies, including the discovery of novel biomarkers, elucidation of disease mechanisms, development of targeted interventions, etc. By integrating multidisciplinary perspectives, this Special Issue aims to advance our understanding of CVD and bridge the gap between molecular research and clinical application, fostering progress in cardiovascular health.

We would like to thank Dr. Cecilia Salzillo from University of Campania “Luigi Vanvitelli", who contributed to and supported the collaboration promotion process and the operation and development of this Special Issue as the assistant of Guest Editor.

Dr. Andrea Marzullo
Guest Editor

Manuscript Submission Information

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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. Current Issues in Molecular Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). 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

  • cardiovascular pathophysiology
  • molecular biomarkers
  • inflammation and oxidative stress
  • therapeutic targets
  • lipid metabolism

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Published Papers (4 papers)

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Research

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26 pages, 10132 KB  
Article
The Role of Oxytocin Neurons in the Paraventricular Nucleus in Chronic-Sleep-Deprivation-Mediated Abnormal Cardiovascular Responses
by Yifei Zhang, Yuxin Wang, Zhendong Xu, Xiangjie Kong, Hairong Wang, Zhibing Lu, Ming Chen and Linlin Bi
Curr. Issues Mol. Biol. 2025, 47(4), 220; https://doi.org/10.3390/cimb47040220 - 25 Mar 2025
Viewed by 2492
Abstract
Sleep disorders increase the risk of cardiovascular diseases. However, the underlying mechanisms remain unclear. This study aims to examine the critical role of oxytocin neurons in the paraventricular nucleus (PVNOXT) in regulating the cardiovascular system and to elucidate potential mechanisms through [...] Read more.
Sleep disorders increase the risk of cardiovascular diseases. However, the underlying mechanisms remain unclear. This study aims to examine the critical role of oxytocin neurons in the paraventricular nucleus (PVNOXT) in regulating the cardiovascular system and to elucidate potential mechanisms through which sleep disturbance may contribute to cardiovascular diseases. In this study, using an automated sleep deprivation system, mice were given chronic sleep deprivation (cSD) for 7 days, 6 h per day. cSD induced blood transcriptomic alterations accompanied by lower heart rate, higher blood pressure, and elevated cardiac autophagy/apoptosis. Instant optogenetic activation of oxytocin neurons in the paraventricular nucleus (PVNOXT) provoked heart rate suppression in normal mice, whereas in cSD mice, activation precipitated intermittent cardiac arrest. On the contrary, inhibition of PVNOXT showed no influence on the cardiovascular system of normal mice, but it attenuated cSD-induced rise in blood pressure. Long-term low-frequency stimulation (LTF) of PVNOXT decreased neuronal excitability and oxytocin release, effectively reversing cSD-mediated cardiovascular responses. Mechanistically, cSD triggered the upregulation of blood-derived 3-mercaptopyruvate sulfurtransferase (mPST), and a suppression of PVNOXT postsynaptic activity to a certain extent. The quick and long-term decrease of oxytocin by LTF could lead to feedback inhibition in mPST expression and thus reverse cSD-mediated cardiovascular responses. Altogether, modulation of PVNOXT could mediate cSD-induced cardiovascular abnormalities without affecting normal mice. Our research provided potential targets and key mechanisms for cardiovascular diseases associated with sleep disorders. Full article
(This article belongs to the Special Issue Cardiovascular Disease: From Molecular Mechanisms to Therapeutic Innovations)
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19 pages, 3783 KB  
Article
Effects of a Three-Day vs. Six-Day Exposure to Normobaric Hypoxia on the Cardiopulmonary Function of Rats
by Charly Bambor, Sarah Daunheimer, Coralie Raffort, Julia Koedel, Aida Salameh and Beate Raßler
Curr. Issues Mol. Biol. 2025, 47(2), 125; https://doi.org/10.3390/cimb47020125 - 14 Feb 2025
Cited by 1 | Viewed by 1799
Abstract
In rats, normobaric hypoxia significantly reduced left ventricular (LV) inotropic function while right ventricular (RV) function was not impaired. In parallel, the animals developed pulmonary edema and inflammation. In the present study, we investigated whether cardiac function and pulmonary injury would aggravate after [...] Read more.
In rats, normobaric hypoxia significantly reduced left ventricular (LV) inotropic function while right ventricular (RV) function was not impaired. In parallel, the animals developed pulmonary edema and inflammation. In the present study, we investigated whether cardiac function and pulmonary injury would aggravate after three and six days of hypoxia exposure or whether cardiopulmonary reactions to prolonged hypoxia would become weaker due to hypoxic acclimatization. Sixty-four female rats were exposed for 72 or 144 h to normoxia. They received a low-rate infusion (0.1 mL/h) with 0.9% NaCl solution. We evaluated indicators of the general condition, blood gas parameters, and hemodynamic function of the rats. In addition, we performed histological and immunohistochemical analyses of the lung. Despite a significant increase in hemoglobin concentration, the LV function deteriorated with prolonged hypoxia. In contrast, the RV systolic pressure and contractility steadily increased by six days of hypoxia. The pulmonary edema and inflammation persisted and rather increased with prolonged hypoxia. Furthermore, elevated protein concentration in the pleural fluid indicated capillary wall stress, which may have aggravated the pulmonary edema. In conclusion, six days of hypoxia and NaCl infusion place significant stress on the cardiopulmonary system of rats, as is also reflected by the 33% of premature deaths in this rat group. Full article
(This article belongs to the Special Issue Cardiovascular Disease: From Molecular Mechanisms to Therapeutic Innovations)
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Review

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28 pages, 2012 KB  
Review
Role of Anti-Inflammatory and Antioxidant Properties of Natural Products in Curing Cardiovascular Diseases
by Amit Kulkarni, Chaitra Chidambar Kulkarni, Seetur Radhakrishna Pradeep, Jagadeesha Poyya, Avinash Kundadka Kudva, Vijay Radhakrishnan and Ajay Sathyanarayanrao Khandagale
Curr. Issues Mol. Biol. 2025, 47(11), 955; https://doi.org/10.3390/cimb47110955 - 17 Nov 2025
Viewed by 1294
Abstract
Cardiovascular diseases (CVDs) remain a leading cause of mortality worldwide. According to the WHO, every year, there is an increase in the rate of death globally due to CVDs, stroke, and myocardial infarction. Several risk factors contribute to the development of CVDs, one [...] Read more.
Cardiovascular diseases (CVDs) remain a leading cause of mortality worldwide. According to the WHO, every year, there is an increase in the rate of death globally due to CVDs, stroke, and myocardial infarction. Several risk factors contribute to the development of CVDs, one of which is hypoxia, defined as a reduction in oxygen levels. This major stressor affects aerobic species and plays a crucial role in the development of cardiovascular disease. Research has uncovered the “hypoxia-inducible factors (HIFs) switch” and investigated the onset, progression, acute and chronic effects, and adaptations of hypoxia, particularly at high altitudes. The hypoxia signalling pathways are closely linked to natural rhythms such as the circadian rhythm and hibernation. In addition to genetic and evolutionary factors, epigenetics also plays an important role in postnatal cardiovascular responses to hypoxia. Oxidized LDL-C initiates atherosclerosis amidst oxidative stress, inflammation, endothelial dysfunction, and vascular remodelling in CVD pathogenesis. Anti-inflammatory and antioxidant biomarkers are needed to identify individuals at risk of cardiovascular events and enhance risk prediction. Among these, C-reactive protein (CRP) is a recognized marker of vascular inflammation in coronary arteries. Elevated pro-atherogenic oxidized LDL (oxLDL) expression serves as an antioxidant marker, predicting coronary heart disease in apparently healthy men. Natural antioxidants and anti-inflammatory molecules protect the heart by reducing oxidative stress, enhancing vasodilation, and improving endothelial function. For instance, the flavonoid quercetin exerts antioxidant and anti-inflammatory effects primarily by activating the Nrf2/HO-1 signaling pathway, thereby enhancing cellular antioxidant defense and reducing reactive oxygen species. Carotenoids, such as astaxanthin, exhibit potent antioxidant activity by scavenging free radicals and preserving mitochondrial integrity. The alkaloid berberine mediates cardiovascular benefits through activation of AMO-activated protein kinase (AMPK) and inhibition of nuclear factor kappa B [NF-kB] signalling, improving lipid metabolism and suppressing inflammatory cytokines. Emerging evidence highlights microRNAs (miRNAs) as potential regulators of oxidative stress via endothelial nitric oxide synthase (eNOS) and silent mating-type information regulation 2 homolog (SIRT1). While the exact mechanisms remain unclear, their benefits are likely to include antioxidant and anti-inflammatory effects, notably reducing the susceptibility of low-density lipoproteins to oxidation. Additionally, the interactions between organs under hypoxia signalling underscore the need for a comprehensive regulatory framework that can support the identification of therapeutic targets, advance clinical research, and enhance treatments, including FDA-approved drugs and those in clinical trials. Promising natural products, including polysaccharides, alkaloids, saponins, flavonoids, and peptides, as well as traditional Indian medicines, have demonstrated anti-hypoxic properties. Their mechanisms of action include increasing haemoglobin, glycogen, and ATP levels, reducing oxidative stress and lipid peroxidation, preserving mitochondrial function, and regulating genes related to apoptosis. These findings emphasise the importance of anti-hypoxia research for the development of effective therapies to combat this critical health problem. A recent approach to controlling CVDs involves the use of antioxidant and anti-inflammatory therapeutics through low-dose dietary supplementation. Despite their effectiveness at low doses, further research on ROS, antioxidants, and nutrition, supported by large multicentre trials, is needed to optimize this strategy. Full article
(This article belongs to the Special Issue Cardiovascular Disease: From Molecular Mechanisms to Therapeutic Innovations)
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15 pages, 2783 KB  
Review
Angiotensin II and Cardiovascular Disease: Balancing Pathogenic and Protective Pathways
by Ulvi Bayraktutan
Curr. Issues Mol. Biol. 2025, 47(7), 501; https://doi.org/10.3390/cimb47070501 - 1 Jul 2025
Cited by 1 | Viewed by 1977
Abstract
The renin-angiotensin-aldosterone system (RAAS) is a hormone system that controls blood pressure and fluid and electrolyte balance. Angiotensin II, a key effector, is produced from angiotensin I by angiotensin-converting enzyme (ACE) and exerts its effects through binding to its type 1 (AT1R) or [...] Read more.
The renin-angiotensin-aldosterone system (RAAS) is a hormone system that controls blood pressure and fluid and electrolyte balance. Angiotensin II, a key effector, is produced from angiotensin I by angiotensin-converting enzyme (ACE) and exerts its effects through binding to its type 1 (AT1R) or type 2 (AT2R) receptors. AT1R activation promotes vasoconstriction, oxidative stress, endothelial dysfunction, peripheral vascular resistance, and atherosclerosis, all of which substantially contribute to cellular senescence and organismal ageing. Conversely, AT2R activation counteracts these effects by inducing vascular relaxation and attenuating vascular cell proliferation and migration, offering protection against occlusive vascular disease. Additionally, conversion of angiotensin II to angiotensin (1-7) or angiotensin I to angiotensin (1-9) by ACE2 provides further cardiovascular protection by lowering oxidative stress, inflammation, and abnormal cell growth. Bearing these in mind, measures to control angiotensin II synthesis or receptor activity have been at the forefront of antihypertensive treatment. This paper briefly reviews the RAAS and explores the dual role of angiotensin II in promoting disease and mediating vascular protection, with a focus on its impact on ageing and cardiovascular pathology. Full article
(This article belongs to the Special Issue Cardiovascular Disease: From Molecular Mechanisms to Therapeutic Innovations)
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