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Life
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Pathogenic Mechanisms, Diagnosis, and Treatment of Hypertension: Insights and Implications
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Pathogenic Mechanisms, Diagnosis, and Treatment of Hypertension: Insights and Implications

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: closed (25 April 2025) | Viewed by 3831

Special Issue Editors

Dr. Shengyu Mu

E-Mail Website
Guest Editor
Department of Pharmacology & Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
Interests: Blood pressure disorder; Hypertension
Dr. Sankar Devarajan

E-Mail Website
Guest Editor
Nutrition and Food Sciences Program, Department of Human Sciences, University of Arkansas at Pine Bluff, Pine Bluff, AK, USA
Interests: diet and nutrition in the prevention of chronic diseases

Special Issue Information

Dear Colleagues

More than one billion people worldwide suffer from hypertension, a leading cause of cardiovascular disease and the primary risk factor for cardiovascular mortality. In the U.S., approximately 670,000 deaths yearly are attributed to hypertension as a primary or contributing cause. Unfortunately, achieving adequate blood pressure control poses a significant challenge, with only around 25% of hypertensive patients in the U.S. attaining normal blood pressure levels through medication regimens. Moreover, discontinuing antihypertensive medications is not an option, even for patients with controlled blood pressure, as sustained elevation tends to recur. These alarming statistics underscore the critical need to identify unknown mechanisms involved in hypertension’s pathogenesis and design improved medications for its treatment. The pathogenesis of hypertension involves an intricate interplay among various systemic regulations within the body, including the renin–angiotensin–aldosterone system (RAAS), vasculature system, renal sodium-fluid regulation system, sympathetic nervous system, metabolic regulation system, immune system, genetic factors, lifestyle factors, and more. This multidimensional perspective highlights the urgency for comprehensive research aimed at unraveling the complexities of hypertension’s mechanisms. Efforts in this direction are essential for the development of advanced diagnostic tools and therapeutic interventions that can effectively address this widespread health challenge. In light of these imperative research needs, we cordially invite the submission of research and review papers contributing to our understanding of hypertension’s pathogenesis and proposing innovative solutions for its diagnosis and treatment. Researchers and experts in the field are encouraged to share their findings and insights, fostering a collaborative effort to advance our capabilities in combating this global health crisis.

Dr. Shengyu Mu
Dr. Sankar Devarajan
Guest Editors

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 2600 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

  • hypertension
  • cardiovascular disease
  • blood pressure
  • pathogenesis

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Published Papers (2 papers)

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Research

11 pages, 2293 KiB  
Article
Hypoxia Modulates Sodium Chloride Co-transporter via CaMKII-β Pathway: An In Vitro Study with mDCT15 Cells
by Lijuan Liang, Kohei Ueda, Sayoko Ogura and Tatsuo Shimosawa
Life 2024, 14(10), 1229; https://doi.org/10.3390/life14101229 - 25 Sep 2024
Viewed by 1432
Abstract
Background: Hypoxia plays a crucial role in regulating various cellular functions, including ion-transport mechanisms in the kidney. The sodium-chloride co-transporter (NCC) is essential for sodium reabsorption in the distal convoluted tubule (DCT). However, the effects of hypoxia on NCC expression and its regulatory [...] Read more.
Background: Hypoxia plays a crucial role in regulating various cellular functions, including ion-transport mechanisms in the kidney. The sodium-chloride co-transporter (NCC) is essential for sodium reabsorption in the distal convoluted tubule (DCT). However, the effects of hypoxia on NCC expression and its regulatory pathways remain unclear. We aimed to explore the effects and potential mechanisms of hypoxia on NCC in vitro. Methods: mDCT15 cells were treated with cobalt chloride (CoCl2) at a concentration of 300 μmol/L to induce hypoxia. The cells were harvested at different time points, namely 30 min, 1 h, 6 h, and 24 h, and the expression of NCC and CaMKII-β was analyzed using Western blot. Results: A time-dependent upregulation of NCC and CaMKII-β expression in response to CoCl2-induced hypoxia. KN93 reversed the effect of CoCl2 on NCC and phosphorylated NCC expression. Conclusions: Hypoxia, mediated through cobalt chloride treatment, upregulates NCC expression via the CaMKII-β pathway in mDCT15 cells. Full article
(This article belongs to the Special Issue Pathogenic Mechanisms, Diagnosis, and Treatment of Hypertension: Insights and Implications)
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21 pages, 9865 KiB  
Article
Esaxerenone Attenuates Aldosterone-Induced Mitochondrial Damage-Mediated Pyroptosis in Mouse Aorta and Rat Vascular Smooth Muscle Cells
by Yunqian Xian, Xuan Wang, Yi Chang, Panpan Qiang, Yutong Han, Juan Hao, Xiaomeng Gao, Tatsuo Shimosawa, Qingyou Xu and Fan Yang
Life 2024, 14(8), 967; https://doi.org/10.3390/life14080967 - 31 Jul 2024
Cited by 2 | Viewed by 1499
Abstract
Background: Vascular smooth muscle cell (VSMC) injury caused by the inflammatory response plays a key role in cardiovascular disease (CVD), and the vasoprotective effects of mineralocorticoid receptor blockers (MRBs) support the role of mineralocorticoid receptor (MR) activation. Methods: C57BL/6 mice and VSMCs isolated [...] Read more.
Background: Vascular smooth muscle cell (VSMC) injury caused by the inflammatory response plays a key role in cardiovascular disease (CVD), and the vasoprotective effects of mineralocorticoid receptor blockers (MRBs) support the role of mineralocorticoid receptor (MR) activation. Methods: C57BL/6 mice and VSMCs isolated from rats were treated with aldosterone and esaxerenone. Caspase-1, GSDMD-N, IL-1β, and NR3C2 expression and DNA damage in aortic VSMCs were detected using immunohistochemistry, Western blotting, and TUNEL staining. Mitochondrial changes were detected by transmission electron microscopy (TEM). Reactive oxygen species (ROS), MitoTracker, JC-I, mitochondrial respiratory chain complexes I–V, and NR3C2 were detected using immunofluorescence and flow cytometry. Pyroptosis was detected with scanning electron microscopy (SEM). Results: After aldosterone treatment, the number of TUNEL-positive cells increased significantly, and the expression of caspase-1, GSDMD-N, and IL-1β increased. TEM revealed mitochondrial damage, and SEM revealed specific pyroptotic changes, such as cell membrane pore changes and cytoplasmic extravasation. Increased ROS levels and nuclear translocation of NR3C2 were also observed. These pyroptosis-related changes were reversed by esaxerenone. Conclusions: Aldosterone activates the MR and mediates mitochondrial damage, thereby inducing pyroptosis in VSMCs via the NLRP3/caspase-1 pathway. Esaxerenone inhibits MR activation and reduces mitochondrial damage and oxidative stress, thereby inhibiting pyroptosis. Full article
(This article belongs to the Special Issue Pathogenic Mechanisms, Diagnosis, and Treatment of Hypertension: Insights and Implications)
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