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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 (31 May 2024) | Viewed by 40217

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Prof. Dr. Edyta Zbroch

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Department of Internal Medicine and Hypertension, Faculty of Medicine, Medical University of Bialystok, 15-089 Bialystok, Poland
Interests: primary and secondary hypertension especially due to renal artery stenosis or kidney disorders; chronic kidney disease; cardiovascular disease; cardiovascular risk factors
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Special Issue Information

Dear Colleagues,

Hypertension (HT) remains the most important risk factor for premature cardiovascular disease (CVD), including stroke, coronary artery disease, heart failure, atrial fibrillation and peripheral vascular disease, as well as for chronic kidney disease (CKD). On the other hand, CKD is an independent risk factor for the development of—often, more severe—coronary artery disease, and CKD is also associated with adverse outcomes in those with existing cardiovascular disease. HT is a very common symptom in patients with CKD. It affects approximately 80 to 85 percent of this population. CVD consistently remains the leading cause of death worldwide; therefore, it is extremally important to know the pathophysiology, molecular mechanisms, and biomarkers of cardiovascular disorders as well as other diseases leading to the development of CVD.

This Special Issues focuses on the pathophysiology, molecular mechanisms, and biomarkers of hypertension and CVD, with particular emphasis on chronic kidney disease, providing better knowledge regarding their development and consequently contributing to more effective prevention, the earliest diagnosis, and thus, appropriate treatment.

We warmly welcome submissions, including original papers and reviews, regarding this widely discussed topic. Data related to molecular mechanisms or pathophysiology are essential, and papers that only contain clinical trials/data are not acceptable.

Prof. Dr. Edyta Zbroch
Guest Editor

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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.

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Keywords

hypertension
hypertension pathophysiology
hypertension molecular mechanisms
cardiovascular disease
cardiovascular pathophysiology
cardiovascular molecular mechanisms
cardiovascular biomarkers
heart failure
coronary artery disease
chronic kidney disease

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Published Papers (9 papers)

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Research

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15 pages, 1955 KiB

Open AccessArticle

The Urinary Glycopeptide Profile Differentiates Early Cardiorenal Risk in Subjects Not Meeting Criteria for Chronic Kidney Disease

by Aranzazu Santiago-Hernandez, Marta Martin-Lorenzo, María Gómez-Serrano, Juan Antonio Lopez, Ariadna Martin-Blazquez, Perceval Vellosillo, Pablo Minguez, Paula J. Martinez, Jesús Vázquez, Gema Ruiz-Hurtado, Maria G. Barderas, Pantelis Sarafidis, Julian Segura, Luis M. Ruilope and Gloria Alvarez-Llamas

Int. J. Mol. Sci. 2024, 25(13), 7005; https://doi.org/10.3390/ijms25137005 - 26 Jun 2024

Cited by 1 | Viewed by 1566

Abstract

Early diagnosis and treatment of chronic kidney disease (CKD) is a worldwide challenge. Subjects with albumin-to-creatinine ratio (ACR) ≥ 30 mg/g and preserved renal function are considered to be at no cardiorenal risk in clinical practice, but prospective clinical studies evidence increased risk, even at the high-normal (HN) ACR range (10–30 mg/g), supporting the need to identify other molecular indicators for early assessment of patients at higher risk. Following our previous studies, here we aim to stratify the normoalbuminuria range according to cardiorenal risk and identify the glycoproteins and N-glycosylation sites associated with kidney damage in subclinical CKD. Glycoproteins were analyzed in urine from hypertensive patients within the HN ACR range compared to control group (C; ACR < 10 mg/g) by mass spectrometry. A different cohort was analyzed for confirmation (ELISA) and sex perspective was evaluated. Patients’ follow-up for 8 years since basal urine collection revealed higher renal function decline and ACR progression for HN patients. Differential N-glycopeptides and their N -glycosylation sites were also identified, together with their pathogenicity. N-glycosylation may condition pathological protein deregulation, and a panel of 62 glycoproteins evidenced alteration in normoalbuminuric subjects within the HN range. Haptoglobin-related protein, haptoglobin, afamin, transferrin, and immunoglobulin heavy constant gamma 1 (IGHG1) and 2 (IGHG2) showed increased levels in HN patients, pointing to disturbed iron metabolism and tubular reabsorption and supporting the tubule as a target of interest in the early progression of CKD. When analyzed separately, haptoglobin, afamin, transferrin, and IGHG2 remained significant in HN, in both women and men. At the peptide level, 172 N-glycopeptides showed differential abundance in HN patients, and 26 showed high pathogenicity, 10 of them belonging to glycoproteins that do not show variation between HN and C groups. This study highlights the value of glycosylation in subjects not meeting KDIGO criteria for CKD. The identified N-glycopeptides and glycosylation sites showed novel targets, for both the early assessment of individual cardiorenal risk and for intervention aimed at anticipating CKD progression. Full article

(This article belongs to the Special Issue Recent Advances in Hypertension and Cardiovascular Disease)

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20 pages, 10330 KiB

Open AccessArticle

Dietary High Salt Intake Exacerbates SGK1-Mediated T Cell Pathogenicity in L-NAME/High Salt-Induced Hypertension

by Dina Maaliki, Maha Itani, Hala Jarrah, Carla El-Mallah, Diana Ismail, Yara E. El Atie, Omar Obeid, Miran A. Jaffa and Hana A. Itani

Int. J. Mol. Sci. 2024, 25(8), 4402; https://doi.org/10.3390/ijms25084402 - 16 Apr 2024

Viewed by 1491

Abstract

Sodium chloride (NaCl) activates Th17 and dendritic cells in hypertension by stimulating serum/glucocorticoid kinase 1 (SGK1), a sodium sensor. Memory T cells also play a role in hypertension by infiltrating target organs and releasing proinflammatory cytokines. We tested the hypothesis that the role of T cell SGK1 extends to memory T cells. We employed mice with a T cell deletion of SGK1, SGK1^fl/fl × tgCD4^cre mice, and used SGK1^fl/fl mice as controls. We treated the mice with L-NAME (0.5 mg/mL) for 2 weeks and allowed a 2-week washout interval, followed by a 3-week high-salt (HS) diet (4% NaCl). L-NAME/HS significantly increased blood pressure and memory T cell accumulation in the kidneys and bone marrow of SGK1^fl/fl mice compared to knockout mice on L-NAME/HS or groups on a normal diet (ND). SGK1^fl/fl mice exhibited increased albuminuria, renal fibrosis, and interferon-γ levels after L-NAME/HS treatment. Myography demonstrated endothelial dysfunction in the mesenteric arterioles of SGK1^fl/fl mice. Bone marrow memory T cells were adoptively transferred from either mouse strain after L-NAME/HS administration to recipient CD45.1 mice fed the HS diet for 3 weeks. Only the mice that received cells from SGK1^fl/fl donors exhibited increased blood pressure and renal memory T cell infiltration. Our data suggest a new therapeutic target for decreasing hypertension-specific memory T cells and protecting against hypertension. Full article

(This article belongs to the Special Issue Recent Advances in Hypertension and Cardiovascular Disease)

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Review

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20 pages, 759 KiB

Open AccessReview

MicroRNA Expression in Patients with Coronary Artery Disease and Hypertension—A Systematic Review

by Bartosz Kondracki, Mateusz Kłoda, Anna Jusiak-Kłoda, Adrianna Kondracka, Jakub Waciński and Piotr Waciński

Int. J. Mol. Sci. 2024, 25(12), 6430; https://doi.org/10.3390/ijms25126430 - 11 Jun 2024

Viewed by 1069

Abstract

Coronary artery disease (CAD) and hypertension significantly contribute to cardiovascular morbidity and mortality. MicroRNAs (miRNAs) have recently emerged as promising biomarkers and therapeutic targets for these conditions. This systematic review conducts a thorough analysis of the literature, with a specific focus on investigating miRNA expression patterns in patients with CAD and hypertension. This review encompasses an unspecified number of eligible studies that employed a variety of patient demographics and research methodologies, resulting in diverse miRNA expression profiles. This review highlights the complex involvement of miRNAs in CAD and hypertension and the potential for advances in diagnostic and therapeutic strategies. Future research endeavors are imperative to validate these findings and elucidate the precise roles of miRNAs in disease progression, offering promising avenues for innovative diagnostic tools and targeted interventions. Full article

(This article belongs to the Special Issue Recent Advances in Hypertension and Cardiovascular Disease)

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21 pages, 1136 KiB

Open AccessReview

On Whether Ca-125 Is the Answer for Diagnosing Overhydration, Particularly in End-Stage Kidney Disease Patients—A Systematic Review

by Barbara Emilia Nikitiuk, Alicja Rydzewska-Rosołowska, Katarzyna Kakareko, Irena Głowińska and Tomasz Hryszko

Int. J. Mol. Sci. 2024, 25(4), 2192; https://doi.org/10.3390/ijms25042192 - 12 Feb 2024

Viewed by 2106

Abstract

Overhydration (OH) is a prevalent medical problem that occurs in patients with kidney failure, but a specific marker has still not been found. Patients requiring kidney replacement therapy suffer from a water imbalance, which is correlated with mortality rates in this population. Currently, clinicians employ techniques such as bioimpedance spectroscopy (BIS) and ultrasound (USG) markers of overhydration or markers of heart and kidney function, namely NT-pro-BNP, GFR, or creatinine levels. New serum markers, including but not limited to Ca-125, galectin-3 (Gal-3), adrenomedullin (AMD), and urocortin-2 (UCN-2), are presently under research and have displayed promising results. Ca-125, which is a protein mainly used in ovarian cancer diagnoses, holds great potential to become an OH marker. It is currently being investigated by cardiologists as it corresponds to the volume status in heart failure (HF) and ventricular hypertrophy, which are also associated with OH. The need to ascertain a more precise marker of overhydration is urgent mainly because physical examinations are exceptionally inaccurate. The signs and symptoms of overhydration, such as edema or a gradual increase in body mass, are not always present, notably in patients with chronic kidney disease. Metabolic disruptions and cachexia can give a false picture of the hydration status. This review paper summarizes the existing knowledge on the assessment of a patient’s hydration status, focusing specifically on kidney diseases and the role of Ca-125. Full article

(This article belongs to the Special Issue Recent Advances in Hypertension and Cardiovascular Disease)

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21 pages, 1371 KiB

Open AccessReview

Elevated Arterial Blood Pressure as a Delayed Complication Following COVID-19—A Narrative Review

by Emilia Bielecka, Piotr Sielatycki, Paulina Pietraszko, Agnieszka Zapora-Kurel and Edyta Zbroch

Int. J. Mol. Sci. 2024, 25(3), 1837; https://doi.org/10.3390/ijms25031837 - 2 Feb 2024

Cited by 2 | Viewed by 3464

Abstract

Arterial hypertension is one of the most common and significant cardiovascular risk factors. There are many well-known and identified risk factors for its development. In recent times, there has been growing concern about the potential impact of COVID-19 on the cardiovascular system and its relation to arterial hypertension. Various theories have been developed that suggest a connection between COVID-19 and elevated blood pressure. However, the precise link between SARS-CoV-2 infection and the long-term risk of developing hypertension remains insufficiently explored. Therefore, the primary objective of our study was to investigate the influence of COVID-19 infection on blood pressure elevation and the subsequent risk of developing arterial hypertension over an extended period. To accomplish this, we conducted a thorough search review of relevant papers in the PubMed and SCOPUS databases up to 3 September 2023. Our analysis encompassed a total of 30 eligible articles. Out of the 30 papers we reviewed, 19 of them provided substantial evidence showing a heightened risk of developing arterial hypertension following COVID-19 infection. Eight of the studies showed that blood pressure values increased after the infection, while three of the qualified studies did not report any notable impact of COVID-19 on blood pressure levels. The precise mechanism behind the development of hypertension after COVID-19 remains unclear, but it is suggested that endothelial injury and dysfunction of the renin–angiotensin–aldosterone system may be contributory. Additionally, changes in blood pressure following COVID-19 infection could be linked to lifestyle alterations that often occur alongside the illness. Our findings emphasize the pressing requirement for thorough research into the relationship between COVID-19 and hypertension. These insights are essential for the development of effective prevention and management approaches for individuals who have experienced COVID-19 infection. Full article

(This article belongs to the Special Issue Recent Advances in Hypertension and Cardiovascular Disease)

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28 pages, 1586 KiB

Open AccessReview

Coatings for Cardiovascular Stents—An Up-to-Date Review

by Alexandru Scafa Udriște, Alexandra Cristina Burdușel, Adelina-Gabriela Niculescu, Marius Rădulescu and Alexandru Mihai Grumezescu

Int. J. Mol. Sci. 2024, 25(2), 1078; https://doi.org/10.3390/ijms25021078 - 16 Jan 2024

Cited by 8 | Viewed by 3588

Abstract

Cardiovascular diseases (CVDs) increasingly burden health systems and patients worldwide, necessitating the improved awareness of current treatment possibilities and the development of more efficient therapeutic strategies. When plaque deposits narrow the arteries, the standard of care implies the insertion of a stent at the lesion site. The most promising development in cardiovascular stents has been the release of medications from these stents. However, the use of drug-eluting stents (DESs) is still challenged by in-stent restenosis occurrence. DESs’ long-term clinical success depends on several parameters, including the degradability of the polymers, drug release profiles, stent platforms, coating polymers, and the metals and their alloys that are employed as metal frames in the stents. Thus, it is critical to investigate new approaches to optimize the most suitable DESs to solve problems with the inflammatory response, delayed endothelialization, and sub-acute stent thrombosis. As certain advancements have been reported in the literature, this review aims to present the latest updates in the coatings field for cardiovascular stents. Specifically, there are described various organic (e.g., synthetic and natural polymer-based coatings, stents coated directly with drugs, and coatings containing endothelial cells) and inorganic (e.g., metallic and nonmetallic materials) stent coating options, aiming to create an updated framework that would serve as an inception point for future research. Full article

(This article belongs to the Special Issue Recent Advances in Hypertension and Cardiovascular Disease)

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17 pages, 1113 KiB

Open AccessReview

Ganglionated Plexus Ablation Procedures to Treat Vasovagal Syncope

by Merav Yarkoni, Wajeeh ur Rehman, Ata Bajwa, Alon Yarkoni and Afzal ur Rehman

Int. J. Mol. Sci. 2023, 24(17), 13264; https://doi.org/10.3390/ijms241713264 - 26 Aug 2023

Cited by 1 | Viewed by 3126

Abstract

Vasovagal syncope (VVS) refers to a heterogeneous group of conditions whereby the cardiovascular reflexes normally controlling the circulation are interrupted irregularly in response to a trigger, resulting in vasodilation, bradycardia, or both. VVS affects one-third of the population at least once in their lifetime or by the age of 60, reduces the quality of life, and may cause disability affecting certain routines. It poses a considerable economic burden on society, and, despite its prevalence, there is currently no proven pharmacological treatment for preventing VVS. The novel procedure of ganglionated plexus (GP) ablation has emerged rapidly in the past two decades, and has been proven successful in treating syncope. Several parameters influence the success rate of GP ablation, including specific ablation sites, localization and surgical techniques, method of access, and the integration of other interventions. This review aims to provide an overview of the existing literature on the physiological aspects and clinical effectiveness of GP ablation in the treatment of VVS. Specifically, we explore the association between GPs and VVS and examine the impact of GP ablation procedures as reported in human clinical trials. Our objective is to shed light on the therapeutic significance of GP ablation in eliminating VVS and restoring normal sinus rhythm, particularly among young adults affected by this condition. Full article

(This article belongs to the Special Issue Recent Advances in Hypertension and Cardiovascular Disease)

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18 pages, 2674 KiB

Open AccessReview

A Systematic Review of the Effect of Vericiguat on Patients with Heart Failure

by Urjosee Sahana, Markus Wehland, Ulf Simonsen, Herbert Schulz and Daniela Grimm

Int. J. Mol. Sci. 2023, 24(14), 11826; https://doi.org/10.3390/ijms241411826 - 23 Jul 2023

Cited by 8 | Viewed by 8617

Abstract

Despite recent advances in heart failure (HF) therapy, the risk of cardiovascular (CV) mortality, morbidity, and HF hospitalization (HFH) are major challenges in HF treatment. We aimed to review the potential of vericiguat as a treatment option for HF. A systematic literature review was performed using the PubMed database and ClinicalTrials.gov. Four randomized controlled trials were identified, which study the safety and efficacy of vericiguat in HF patients. Vericiguat activates soluble guanylate cyclase (sGC) by binding to the beta-subunit, bypassing the requirement for NO-induced activation. The nitric oxide (NO)–sGC–cyclic guanosine monophosphate (cGMP) pathway plays an essential role in cardiovascular (CV) regulation and the protection of healthy cardiac function but is impaired in HF. Vericiguat reduced the risk of CV death and HFH in HF patients with reduced ejection fraction (HFrEF) but showed no therapeutic effect on HF with preserved ejection fraction (HFpEF). The trials demonstrated a favorable safety profile with most common adverse events such as hypotension, syncope, and anemia. Therefore, vericiguat is recommended for patients with HFrEF and a minimum systolic blood pressure of 100 mmHg. Treatment with vericiguat is considered when the individual patient experiences decompensation despite being on guideline-recommended medication, e.g., angiotensin-converting inhibitor/AT1 receptor antagonist, beta-adrenoceptor antagonist, spironolactone, and sodium-glucose transporter 2 inhibitors. Furthermore, larger studies are required to investigate any potential effect of vericiguat in HFpEF patients. Despite the limitations, vericiguat can be recommended for patients with HFrEF, where standard-of-care is insufficient, and the disease worsens. Full article

(This article belongs to the Special Issue Recent Advances in Hypertension and Cardiovascular Disease)

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14 pages, 549 KiB

Open AccessReview

Chronic Kidney Disease as a Comorbidity in Heart Failure

by Magdalena Szlagor, Jill Dybiec, Ewelina Młynarska, Jacek Rysz and Beata Franczyk

Int. J. Mol. Sci. 2023, 24(3), 2988; https://doi.org/10.3390/ijms24032988 - 3 Feb 2023

Cited by 28 | Viewed by 14002

Abstract

Heart failure (HF) is one of the greatest problems in healthcare and it often coexists with declining renal function. The pathophysiology between the heart and the kidneys is bidirectional. Common mechanisms leading to the dysfunction of these organs result in a vicious cycle of cardiorenal deterioration. It is also associated with difficulties in the treatment of aggravating HF and chronic kidney disease (CKD) and, as a consequence, recurrent hospitalizations and death. As the worsening of renal function has an undeniably negative impact on the outcomes in patients with HF, searching for new treatment strategies and identification of biomarkers is necessary. This review is focused on the pathomechanisms in chronic kidney disease in patients with HF and therapeutic strategies for co-existing CKD and HF. Full article

(This article belongs to the Special Issue Recent Advances in Hypertension and Cardiovascular Disease)

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