Special Issue "Cardiovascular Medicine: From Bench to Bedside"

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (30 November 2021).

Special Issue Editor

Dr. Benedetta Porro
E-Mail Website
Guest Editor
IRCCS Centro Cardiologico Monzino, Milan, Italy
Interests: cardiovascular disease; oxidative stress; endothelial dysfunction, red blood cell; metabolomics; pharmacometabolomics; liquid chromatography-tandem mass spectrometry

Special Issue Information

Dear Colleagues,

Cardiovascular disease (CVD) is a leading cause of deaths worldwide, with deaths due to atherothrombosis expected to increase yearly from 17.3 to 23.6 million by 2030.  In the recent years, constant progresses in medical research, in parallel to the development of new techniques, have allowed better descriptions of the complex network of factors that are involved and cumulatively interact in the onset of the atherosclerotic phenomenon and in its progression. In this field, the improvement of omics approaches is helping to unravel the role of new and already known processes related to CVD development (e.g., oxidative stress, endothelial dysfunction, inflammation, fatty acid oxidation) beyond traditional risk factors. This is crucial for the development of innovative strategies in CVD prevention (including novel laboratory technologies to explore metabolic alterations and molecular studies of predisposition genes) and treatment. To identify appropriate targets in CVD prevention and treatment, the most advanced research information in the area field should be gathered and related or translated to practical (clinical and pathophysiological) questions. This is the aim and purpose of the present Special Issue of the journal.

Dr. Benedetta Porro
Guest Editor

Manuscript Submission Information

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Keywords

  • cardiovascular disease
  • oxidative stress
  • endothelial dysfunction
  • red blood cell
  • circulating biomarker
  • liquid chromatography-tandem mass spectrometry

Published Papers (3 papers)

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Research

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Article
GJA1 Expression and Left Atrial Remodeling in the Incidence of Atrial Fibrillation in Patients with Obstructive Sleep Apnea Syndrome
Biomedicines 2021, 9(10), 1463; https://doi.org/10.3390/biomedicines9101463 - 13 Oct 2021
Viewed by 372
Abstract
Obstructive sleep apnea syndrome (OSAS) is an important risk factor for atrial fibrillation (AF). GJA1 gene encoding connexin43, a major protein in cardiac gap junctions, plays a crucial role in the synchronized contraction of the heart and in cardiac arrhythmia. However, little is [...] Read more.
Obstructive sleep apnea syndrome (OSAS) is an important risk factor for atrial fibrillation (AF). GJA1 gene encoding connexin43, a major protein in cardiac gap junctions, plays a crucial role in the synchronized contraction of the heart and in cardiac arrhythmia. However, little is known regarding the role of GJA1 expression in the incidence of AF in patients with OSAS. All prospectively enrolled OSAS patients underwent polysomnography, electrocardiography, a 24-h Holter test, and echocardiography. Moderate-to-severe OSAS was defined as an apnea-hypopnea index (AHI) ≥ 15. Exosomes were purified from the plasma of all OSAS patients and incubated in HL-1 cells to investigate the effect of exosomes from patients with and without AF on GJA1 expression. A total of 129 patients were recruited for this study; 26 were excluded due to an AHI < 15. Of the 103 enrolled patients, 21 had AF, and 82 did not. Multivariate analysis showed diabetes mellitus, lower sleep efficiency, lower left ventricular ejection fraction, and larger left atrial (LA) size were independent predictors of AF occurrence in OSAS patients. The area under the receiver operating characteristic curve for LA with a size ≥38.5 mm for predicting AF occurrence in OSAS patients was 0.795 (95% confidence interval [0.666, 0.925]); p < 0.001). GJA1 expression in HL-1 cells incubated with exosomes from OSAS patients with AF was lower than that with exosomes from patients without AF after controlling for age and sex and was negatively correlated with the AHI and oxygen desaturation index (ODI), especially during the non-rapid eye movement period (NREM) of OSAS patients with AF (all p < 0.05). LA size was an independent predictor of AF occurrence in OSAS patients. The AHI and ODI in the NREM period of OSAS patients with AF were negatively correlated with GJA1 expression in HL-1 cells, which offers a hint that GJA1 may play a crucial role in the development of AF in patients with OSAS. Full article
(This article belongs to the Special Issue Cardiovascular Medicine: From Bench to Bedside)
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Article
Long Term Response to Circulating Angiogenic Cells, Unstimulated or Atherosclerotic Pre-Conditioned, in Critical Limb Ischemic Mice
Biomedicines 2021, 9(9), 1147; https://doi.org/10.3390/biomedicines9091147 - 03 Sep 2021
Viewed by 539
Abstract
Critical limb ischemia (CLI), the most severe form of peripheral artery disease, results from the blockade of peripheral vessels, usually correlated to atherosclerosis. Currently, endovascular and surgical revascularization strategies cannot be applied to all patients due to related comorbidities, and even so, most [...] Read more.
Critical limb ischemia (CLI), the most severe form of peripheral artery disease, results from the blockade of peripheral vessels, usually correlated to atherosclerosis. Currently, endovascular and surgical revascularization strategies cannot be applied to all patients due to related comorbidities, and even so, most patients require re-intervention or amputation within a year. Circulating angiogenic cells (CACs) constitute a good alternative as CLI cell therapy due to their vascular regenerative potential, although the mechanisms of action of these cells, as well as their response to pathological conditions, remain unclear. Previously, we have shown that CACs enhance angiogenesis/arteriogenesis from the first days of administration in CLI mice. Also, the incubation ex vivo of these cells with factors secreted by atherosclerotic plaques promotes their activation and mobilization. Herein, we have evaluated the long-term effect of CACs administration in CLI mice, whether pre-stimulated or not with atherosclerotic factors. Remarkably, mice receiving CACs and moreover, pre-stimulated CACs, presented the highest blood flow recovery, lower progression of ischemic symptoms, and decrease of immune cells recruitment. In addition, many proteins potentially involved, like CD44 or matrix metalloproteinase 9 (MMP9), up-regulated in response to ischemia and decreased after CACs administration, were identified by a quantitative proteomics approach. Overall, our data suggest that pre-stimulation of CACs with atherosclerotic factors might potentiate the regenerative properties of these cells in vivo. Full article
(This article belongs to the Special Issue Cardiovascular Medicine: From Bench to Bedside)
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Review

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Review
Catestatin as a Biomarker of Cardiovascular Diseases: A Clinical Perspective
Biomedicines 2021, 9(12), 1757; https://doi.org/10.3390/biomedicines9121757 - 25 Nov 2021
Viewed by 212
Abstract
Accounting for almost one-third of the global mortality, cardiovascular diseases (CVDs) represent a major global health issue. Emerging data suggest that most of the well-established mechanistic explanations regarding the cardiovascular pathophysiology are flawed, and cannot fully explain the progression and long-term effects of [...] Read more.
Accounting for almost one-third of the global mortality, cardiovascular diseases (CVDs) represent a major global health issue. Emerging data suggest that most of the well-established mechanistic explanations regarding the cardiovascular pathophysiology are flawed, and cannot fully explain the progression and long-term effects of these diseases. On the other hand, dysregulation of the sympathetic nervous system (SNS) has emerged as an important player in the pathophysiology of CVDs. Even though upregulated SNS activity is an essential compensatory response to various stress conditions, in the long term, it becomes a major contributor to both cardiac dysfunction and vascular damage. Despite the fact that the importance of SNS hyperactivity in the setting of CVDs has been well-appreciated, its exact quantification and clinical application in either diagnostics or therapy of CVDs is still out of reach. Nevertheless, in recent years a number of novel laboratory biomarkers implicated in the pathophysiology of SNS activation have been explored. Specifically, in this review, we aimed to discuss the role of catestatin, a potent physiological inhibitor of catecholamine spillover that offers cardioprotective effects. Limited data indicate that catestatin could also be a reliable indirect marker of SNS activity and it is likely that high CST levels reflect advanced CV disease burden. Consequently, large-scale studies are required to validate these observations in the upcoming future. Full article
(This article belongs to the Special Issue Cardiovascular Medicine: From Bench to Bedside)
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