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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: 30 June 2025 | Viewed by 1298

Special Issue Editor


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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
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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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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 (2 papers)

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Research

26 pages, 10132 KiB  
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 273
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
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19 pages, 3783 KiB  
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
Viewed by 767
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
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