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Cardiovascular Endocrinology Research
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Cardiovascular Endocrinology Research

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 October 2023) | Viewed by 15354

Special Issue Editor

Dr. José Ricardo Romero

E-Mail Website
Guest Editor
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA
Interests: cardiovascular endocrinology; salt-sensitive blood pressure; hypertension; inflammatory responses; diabetes; thrombosis; aldosterone; ion transport; magnesium; mineralocorticoid receptor; renin-angiotensin-aldosterone system; biological sex; striatin; caveolin; endoplasmic reticulum amino peptidase; blood cells; endothelium; adrenal gland; vasculature; kidney; heart

Special Issue Information

Dear Colleagues, 

Significant advances in our molecular understanding of cardiovascular diseases have occurred in the past several decades. However, cardiovascular diseases remain a leading cause of death in women and men worldwide. The incidence of cardiovascular diseases is commonly reported to be greater in men than women. However, women have higher morbidity and mortality than men following cardiovascular events such as stroke and heart attacks through signaling mechanisms that remain unresolved. Growing evidence shows that hormonal dysregulation, renal dysfunction, metabolic disturbances, and biological sex contribute to cardiovascular diseases through signaling pathways that remain unclear. In this Special Issue titled Cardiovascular Endocrinology Research 2022, we will collect a series of studies that will provide novel insight while improving our understanding of novel molecular and therapeutic targets and signaling molecules mediating cardiovascular diseases and hormonal interactions in women and men.

Dr. José Ricardo Romero
Guest Editor

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

  • sex hormones
  • inflammatory molecules
  • renin
  • angiotensin
  • aldosterone
  • estradiol
  • testosterone
  • cortisol
  • endocrinology
  • vascular disease
  • hypertension
  • blood pressure
  • diabetes

Published Papers (5 papers)

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Research

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25 pages, 20264 KiB  
Article
The Triad Na+ Activated Na+ Channel (Nax)—Salt Inducible KINASE (SIK) and (Na+ + K+)-ATPase: Targeting the Villains to Treat Salt Resistant and Sensitive Hypertension
by Sabrina R. Gonsalez, Dayene S. Gomes, Alessandro M. de Souza, Fernanda M. Ferrão, Zoe Vallotton, Venkateswara R. Gogulamudi, Jennifer Lowe, Dulce E. Casarini, Minolfa C. Prieto and Lucienne S. Lara
Int. J. Mol. Sci. 2023, 24(9), 7887; https://doi.org/10.3390/ijms24097887 - 26 Apr 2023
Cited by 1 | Viewed by 1506
Abstract
The Na+-activated Na+ channel (Nax) and salt-inducible kinase (SIK) are stimulated by increases in local Na+ concentration, affecting (Na+ + K+)-ATPase activity. To test the hypothesis that the triad Nax/SIK/(Na+ + K+)-ATPase contributes [...] Read more.
The Na+-activated Na+ channel (Nax) and salt-inducible kinase (SIK) are stimulated by increases in local Na+ concentration, affecting (Na+ + K+)-ATPase activity. To test the hypothesis that the triad Nax/SIK/(Na+ + K+)-ATPase contributes to kidney injury and salt-sensitive hypertension (HTN), uninephrectomized male Wistar rats (200 g; n = 20) were randomly divided into 4 groups based on a salt diet (normal salt diet; NSD—0.5% NaCl—or high-salt diet; HSD—4% NaCl) and subcutaneous administration of saline (0.9% NaCl) or deoxycorticosterone acetate (DOCA, 8 mg/kg), as follows: Control (CTRL), CTRL-Salt, DOCA, and DOCA-Salt, respectively. After 28 days, the following were measured: kidney function, blood pressure, (Na+ + K+)-ATPase and SIK1 kidney activities, and Nax and SIK1 renal expression levels. SIK isoforms in kidneys of CTRL rats were present in the glomerulus and tubular epithelia; they were not altered by HSD and/or HTN. CTRL-Salt rats remained normotensive but presented slight kidney function decay. HSD rats displayed augmentation of the Nax/SIK/(Na+ + K+)-ATPase pathway. HTN, kidney injury, and kidney function decay were present in all DOCA rats; these were aggravated by HSD. DOCA rats presented unaltered (Na+ + K+)-ATPase activity, diminished total SIK activity, and augmented SIK1 and Nax content in the kidney cortex. DOCA-Salt rats expressed SIK1 activity and downregulation in (Na+ + K+)-ATPase activity in the kidney cortex despite augmented Nax content. The data of this study indicate that the (Na+ + K+)-ATPase activity response to SIK is attenuated in rats under HSD, independent of HTN, as a mechanism contributing to kidney injury and salt-sensitive HTN. Full article
(This article belongs to the Special Issue Cardiovascular Endocrinology Research)
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19 pages, 4713 KiB  
Article
Effects of Mineralocorticoid Receptor Blockade and Statins on Kidney Injury Marker 1 (KIM-1) in Female Rats Receiving L-NAME and Angiotensin II
by Jiayan Huang, Ezgi Caliskan Guzelce, Shadi K. Gholami, Kara L. Gawelek, Richard N. Mitchell, Luminita H. Pojoga, Jose R. Romero, Gordon H. Williams and Gail K. Adler
Int. J. Mol. Sci. 2023, 24(7), 6500; https://doi.org/10.3390/ijms24076500 - 30 Mar 2023
Cited by 1 | Viewed by 2112
Abstract
Kidney injury molecule-1 (KIM-1) is a biomarker of renal injury and a predictor of cardiovascular disease. Aldosterone, via activation of the mineralocorticoid receptor, is linked to cardiac and renal injury. However, the impact of mineralocorticoid receptor activation and blockade on KIM-1 is uncertain. [...] Read more.
Kidney injury molecule-1 (KIM-1) is a biomarker of renal injury and a predictor of cardiovascular disease. Aldosterone, via activation of the mineralocorticoid receptor, is linked to cardiac and renal injury. However, the impact of mineralocorticoid receptor activation and blockade on KIM-1 is uncertain. We investigated whether renal KIM-1 is increased in a cardiorenal injury model induced by L-NAME/ANG II, and whether mineralocorticoid receptor blockade prevents the increase in KIM-1. Since statin use is associated with lower aldosterone, we also investigated whether administering eiSther a lipophilic statin (simvastatin) or a hydrophilic statin (pravastatin) prevents the increase in renal KIM-1. Female Wistar rats (8–10 week old), consuming a high salt diet (1.6% Na+), were randomized to the following conditions for 14 days: control; L-NAME (0.2 mg/mL in drinking water)/ANG II (225 ug/kg/day on days 12–14); L-NAME/ANG II + eplerenone (100 mg/kg/day p.o.); L-NAME/ANG II + pravastatin (20 mg/kg/day p.o.); L-NAME/ANG II + simvastatin (20 mg/kg/day p.o.). Groups treated with L-NAME/ANG II had significantly higher blood pressure, plasma and urine aldosterone, cardiac injury/stroke composite score, and renal KIM-1 than the control group. Both eplerenone and simvastatin reduced 24-h urinary KIM-1 (p = 0.0046, p = 0.031, respectively) and renal KIM-1 immunostaining (p = 0.004, p = 0.037, respectively). Eplerenone also reduced renal KIM-1 mRNA expression (p = 0.012) and cardiac injury/stroke composite score (p = 0.04). Pravastatin did not affect these damage markers. The 24-h urinary KIM-1, renal KIM-1 immunostaining, and renal KIM-1 mRNA expression correlated with cardiac injury/stroke composite score (p < 0.0001, Spearman ranked correlation = 0.69, 0.66, 0.59, respectively). In conclusion, L-NAME/ANG II increases renal KIM-1 and both eplerenone and simvastatin blunt this increase in renal KIM-1. Full article
(This article belongs to the Special Issue Cardiovascular Endocrinology Research)
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11 pages, 1931 KiB  
Article
Disordered Glucose Levels Are Associated with Xanthine Oxidase Activity in Overweight Type 2 Diabetic Women
by Maria Elena Hernandez-Hernandez, Enrique Torres-Rasgado, Patricia Pulido-Perez, Leticia Nicolás-Toledo, Margarita Martínez-Gómez, Jorge Rodríguez-Antolín, Ricardo Pérez-Fuentes and Jose R. Romero
Int. J. Mol. Sci. 2022, 23(19), 11177; https://doi.org/10.3390/ijms231911177 - 23 Sep 2022
Cited by 5 | Viewed by 1941
Abstract
Oxidative stress plays an important role in vascular complications observed in patients with obesity and Type 2 Diabetes (T2D). Xanthine oxidase (XO) breaks down purine nucleotides into uric acid and contributes to the production of reactive oxygen species (ROS). However, the relationship between [...] Read more.
Oxidative stress plays an important role in vascular complications observed in patients with obesity and Type 2 Diabetes (T2D). Xanthine oxidase (XO) breaks down purine nucleotides into uric acid and contributes to the production of reactive oxygen species (ROS). However, the relationship between XO activity and glucose homeostasis in T2D subjects with obesity is unclear. We hypothesized that disordered glucose levels are associated with serum XO activity in overweight women and men with T2D and without hyperuricemia. We studied serum XO activity in women and men with and without T2D. Our results show that serum XO activity was greater in T2D patients with body mass index (BMI) ≥ 25 kg/m2 than in those with BMI < 25 kg/m2 (p < 0.0001). Sex-based comparative analyses of overweight T2D patients showed that serum XO activity correlated with homeostasis model assessment of β-cell function (HOMA-β), fasting plasma glucose (FPG), and hemoglobin A1C in overweight T2D women but not in overweight T2D men. In addition, as compared to overweight T2D men, women had higher high-sensitivity C-reactive protein (hs-CRP) levels. However, overweight T2D men had higher XO activity and uric acid levels than women. Our results suggest that XO activity is higher in overweight T2D patients, especially in men, but is more sensitive to disordered glucose levels in overweight women with T2D. Full article
(This article belongs to the Special Issue Cardiovascular Endocrinology Research)
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Review

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11 pages, 823 KiB  
Review
Pathophysiology and Management of Glycemic Alterations before and after Surgery for Pheochromocytoma and Paraganglioma
by Chiara Lopez, Chiara Bima, Martina Bollati, Fabio Bioletto, Matteo Procopio, Stefano Arata, Daniele Giuseppe Candela, Guglielmo Beccuti, Ezio Ghigo, Mauro Maccario and Mirko Parasiliti-Caprino
Int. J. Mol. Sci. 2023, 24(6), 5153; https://doi.org/10.3390/ijms24065153 - 8 Mar 2023
Cited by 3 | Viewed by 3360
Abstract
Glycemic alterations are frequent in patients with pheochromocytoma and paraganglioma (PPGL), but the real incidence of secondary diabetes mellitus (DM) is uncertain, because prospective multicenter studies on this topic are lacking in the literature. The main pathophysiological mechanisms of glucose homeostasis alterations in [...] Read more.
Glycemic alterations are frequent in patients with pheochromocytoma and paraganglioma (PPGL), but the real incidence of secondary diabetes mellitus (DM) is uncertain, because prospective multicenter studies on this topic are lacking in the literature. The main pathophysiological mechanisms of glucose homeostasis alterations in PPGL, related to catecholamine hypersecretion, are impaired insulin and glucagon-like peptide type 1 (GLP-1) secretion and increased insulin resistance. Moreover, it has been reported that different pathways leading to glucose intolerance may be related to the secretory phenotype of the chromaffin tumor. Predictive factors for the development of glucose intolerance in PPGL patients are a higher age at diagnosis, the need for a higher number of anti-hypertensive drugs, and the presence of secreting neoplasms. Tumor resection is strongly related to the resolution of DM in PPGL patients, with a significant improvement of glycemic control in most cases. We can hypothesize a different personalized therapeutic approach based on the secretory phenotype. The adrenergic phenotype is more closely related to reduced insulin secretion, so insulin therapy may be required. On the other hand, the noradrenergic phenotype mainly acts by increasing insulin resistance and, therefore, insulin-sensitizing antidiabetic agents can find a greater application. Regarding GLP-1 receptor agonists, the data suggest a possible promising therapeutic effect, based on the assumption that GLP-1 secretion is impaired in patients with PPGL. The principal predictors of remission of glycemic alterations after surgery for PPGL are a lower preoperative body mass index (BMI), a larger tumor, higher preoperative catecholamine levels, and a shorter duration of the disease (under three years). Otherwise, after resection of PPGL, hypoglycemia can occur as the result of an excessive rebound of preoperative hyperinsulinemia. It is a rare, but potentially severe complication reported in a lot of case reports and a few small retrospective studies. Higher 24-h urinary metanephrine levels, longer operative times and larger tumors are predictive factors for hypoglycemia in this setting. In conclusion, alterations of carbohydrate metabolism are clinically relevant manifestations of PPGL before and after surgery, but there is the need to conduct multicenter prospective studies to obtain an adequate sample size, and to allow the creation of shared strategies for the clinical management of these potentially severe manifestations of PPGL. Full article
(This article belongs to the Special Issue Cardiovascular Endocrinology Research)
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20 pages, 2076 KiB  
Review
NLRP3 Inflammasome/Pyroptosis: A Key Driving Force in Diabetic Cardiomyopathy
by Lixia Zhang, Chenchen Ai, Ming Bai, Jinglei Niu and Zheng Zhang
Int. J. Mol. Sci. 2022, 23(18), 10632; https://doi.org/10.3390/ijms231810632 - 13 Sep 2022
Cited by 19 | Viewed by 5489
Abstract
Diabetic cardiomyopathy (DCM), a serious diabetic complication, is a kind of low-grade inflammatory cardiovascular disorder. Due to the high risk of morbidity and mortality, DCM has demanded the attention of medical researchers worldwide. The pathophysiological nature of DCM is intricate, and the genesis [...] Read more.
Diabetic cardiomyopathy (DCM), a serious diabetic complication, is a kind of low-grade inflammatory cardiovascular disorder. Due to the high risk of morbidity and mortality, DCM has demanded the attention of medical researchers worldwide. The pathophysiological nature of DCM is intricate, and the genesis and development of which are a consequence of the coaction of many factors. However, the exact pathogenesis mechanism of DCM remains unclear. Pyroptosis is a newly identified programmed cell death (PCD) that is directly related to gasdermin D(GSDMD). It is characterized by pore formation on the cell plasma membrane, the release of inflammatory mediators, and cell lysis. The initiation of pyroptosis is closely correlated with NOD-like receptor 3 (NLRP3) activation, which activates caspase-1 and promotes the cleaving of GSDMD. In addition to adjusting the host’s immune defense, NLRP3 inflammasome/pyroptosis plays a critical role in controlling the systemic inflammatory response. Recent evidence has indicated that NLRP3 inflammasome/pyroptosis has a strong link with DCM. Targeting the activation of NLRP3 inflammasome or pyroptosis may be a hopeful therapeutic strategy for DCM. The focus of this review is to summarize the relevant mechanisms of pyroptosis and the relative contributions in DCM, highlighting the potential therapeutic targets in this field. Full article
(This article belongs to the Special Issue Cardiovascular Endocrinology Research)
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