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Emerging Treatment for Cardiovascular Diseases
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Emerging Treatment for Cardiovascular Diseases

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 (20 December 2022) | Viewed by 13035

Special Issue Editor

Prof. Dr. Steve Leu

E-Mail Website
Guest Editor
Institute for Translational Research in Biomedicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan
Interests: cardiovascular disease; stem cell therapy; maternal nutrition and fetal development

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVDs), a group of disorders of the heart and vessels as well as their associated adverse conditions, are the leading cause of death globally. An estimated 17.9 million people died from CVDs in 2019, representing 32% of all deaths worldwide. Despite significant progress in treatments of CVDs, there remains a challenge for designing therapeutic strategies with better effectiveness and without unnecessary complications. Furthermore, organ crosstalk further complicates the design and choice of treatments for CVDs. In addition to traditional pharmacotherapy and surgical intervention, molecular and cellular therapies such as miRNA and stem cells have been considered as potential approaches to promote functional recovery and improve the prognosis of patients with CVDs.

This Special Issue on “Emerging Treatment for Cardiovascular Diseases” aims to curate advances in developing and validating therapeutic strategies for CVDs. We would like to invite reviews and original articles on, but not limited to, the following topics:

  • The development and validation of potential therapeutic approaches (e.g., nucleic acid therapy, cell therapy, synthetic chemicals, antibodies, and mechanical force) in pre-clinical animal models of cardiovascular diseases.
  • Improvements in the therapeutic efficacy of current treatments for cardiovascular diseases.
  • Mechanistic investigations into and the designing of therapeutic strategies against crosstalk between cardiovascular diseases and other organ systems, such as the nervous, endocrine, metabolic, renal, and immune systems.

Dr. Steve Leu
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

  • cardiovascular diseases
  • ischemic injury
  • metabolic syndrome
  • organ crosstalk
  • pathogenesis and treatment
  • cell therapy
  • combination therapy

Published Papers (5 papers)

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Research

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17 pages, 2502 KiB  
Article
The Novel Cardiac Myosin Activator Danicamtiv Improves Cardiac Systolic Function at the Expense of Diastolic Dysfunction In Vitro and In Vivo: Implications for Clinical Applications
by Arnold Péter Ráduly, Fruzsina Sárkány, Máté Balázs Kovács, Brigitta Bernát, Béla Juhász, Zoltán Szilvássy, Róbert Porszász, Balázs Horváth, Norbert Szentandrássy, Péter Nánási, Zoltán Csanádi, István Édes, Attila Tóth, Zoltán Papp, Dániel Priksz and Attila Borbély
Int. J. Mol. Sci. 2023, 24(1), 446; https://doi.org/10.3390/ijms24010446 - 27 Dec 2022
Cited by 6 | Viewed by 2884
Abstract
Recent cardiotropic drug developments have focused on cardiac myofilaments. Danicamtiv, the second direct myosin activator, has achieved encouraging results in preclinical and clinical studies, thus implicating its potential applicability in the treatment of heart failure with reduced ejection fraction (HFrEF). Here, we analyzed [...] Read more.
Recent cardiotropic drug developments have focused on cardiac myofilaments. Danicamtiv, the second direct myosin activator, has achieved encouraging results in preclinical and clinical studies, thus implicating its potential applicability in the treatment of heart failure with reduced ejection fraction (HFrEF). Here, we analyzed the inotropic effects of danicamtiv in detail. To this end, changes in sarcomere length and intracellular Ca2+ levels were monitored in parallel, in enzymatically isolated canine cardiomyocytes, and detailed echocardiographic examinations were performed in anesthetized rats in the absence or presence of danicamtiv. The systolic and diastolic sarcomere lengths decreased; contraction and relaxation kinetics slowed down with increasing danicamtiv concentrations without changes in intracellular Ca2+ transients in vitro. Danicamtiv evoked remarkable increases in left ventricular ejection fraction and fractional shortening, also reflected by changes in systolic strain. Nevertheless, the systolic ejection time was significantly prolonged, the ratio of diastolic to systolic duration was reduced, and signs of diastolic dysfunction were also observed upon danicamtiv treatment in vivo. Taken together, danicamtiv improves cardiac systolic function, but it can also limit diastolic performance, especially at high drug concentrations. Full article
(This article belongs to the Special Issue Emerging Treatment for Cardiovascular Diseases)
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21 pages, 10450 KiB  
Article
Platelet–Neutrophil Association in NETs-Rich Areas in the Retrieved AIS Patient Thrombi
by Ghulam Jeelani Pir, Aijaz Parray, Raheem Ayadathil, Sajitha V. Pananchikkal, Fayaz Ahmad Mir, Islam Muhammad, Ahmed Abubakar, Nueman Amir, Sohail Hussain, Khawaja H. Haroon, Ahmad Muhammad, Yahya Imam, Satya Narayana Patro, Naveed Akhtar, Aymen Zakaria and Saadat Kamran
Int. J. Mol. Sci. 2022, 23(22), 14477; https://doi.org/10.3390/ijms232214477 - 21 Nov 2022
Cited by 5 | Viewed by 2433
Abstract
Histological structure of thrombi is a strong determinant of the outcome of vascular recanalization therapy, the only treatment option for acute ischemic stroke (AIS) patients. A total of 21 AIS patients from this study after undergoing non-enhanced CT scan and multimodal MRI were [...] Read more.
Histological structure of thrombi is a strong determinant of the outcome of vascular recanalization therapy, the only treatment option for acute ischemic stroke (AIS) patients. A total of 21 AIS patients from this study after undergoing non-enhanced CT scan and multimodal MRI were treated with mechanical stent-based and manual aspiration thrombectomy, and thromboembolic retrieved from a cerebral artery. Complementary histopathological and imaging analyses were performed to understand their composition with a specific focus on fibrin, von Willebrand factor, and neutrophil extracellular traps (NETs). Though distinct RBC-rich and platelet-rich areas were found, AIS patient thrombi were overwhelmingly platelet-rich, with 90% of thrombi containing <40% total RBC-rich contents (1.5 to 37%). Structurally, RBC-rich areas were simple, consisting of tightly packed RBCs in thin fibrin meshwork with sparsely populated nucleated cells and lacked any substantial von Willebrand factor (VWF). Platelet-rich areas were structurally more complex with thick fibrin meshwork associated with VWF. Plenty of leukocytes populated the platelet-rich areas, particularly in the periphery and border areas between platelet-rich and RBC-rich areas. Platelet-rich areas showed abundant activated neutrophils (myeloperoxidase+ and neutrophil-elastase+) containing citrullinated histone-decorated DNA. Citrullinated histone-decorated DNA also accumulated extracellularly, pointing to NETosis by the activated neutrophils. Notably, NETs-containing areas showed strong reactivity to VWF, platelets, and high-mobility group box 1 (HMGB1), signifying a close interplay between these components. Full article
(This article belongs to the Special Issue Emerging Treatment for Cardiovascular Diseases)
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12 pages, 7529 KiB  
Article
Lithium Treatment Improves Cardiac Dysfunction in Rats Deprived of Rapid Eye Movement Sleep
by Pao-Huan Chen, Cheng-Chih Chung, Shuen-Hsin Liu, Yu-Hsun Kao and Yi-Jen Chen
Int. J. Mol. Sci. 2022, 23(19), 11226; https://doi.org/10.3390/ijms231911226 - 23 Sep 2022
Cited by 4 | Viewed by 1861
Abstract
Rapid eye movement (REM) sleep deprivation triggers mania and induces cardiac fibrosis. Beyond neuroprotection, lithium has cardioprotective potential and antifibrotic activity. This study investigated whether lithium improved REM sleep deprivation-induced cardiac dysfunction and evaluated the potential mechanisms. Transthoracic echocardiography, histopathological analysis, and Western [...] Read more.
Rapid eye movement (REM) sleep deprivation triggers mania and induces cardiac fibrosis. Beyond neuroprotection, lithium has cardioprotective potential and antifibrotic activity. This study investigated whether lithium improved REM sleep deprivation-induced cardiac dysfunction and evaluated the potential mechanisms. Transthoracic echocardiography, histopathological analysis, and Western blot analysis were performed in control and REM sleep-deprived rats with or without lithium treatment (LiCl of 1 mmol/kg/day administered by oral gavage for 4 weeks) in vivo and in isolated ventricular preparations. The results revealed that REM sleep-deprived rats exhibited impaired contractility and greater fibrosis than control and lithium-treated REM sleep-deprived rats. Western blot analysis showed that REM sleep-deprived hearts had higher expression levels of transforming growth factor beta (TGF-β), phosphorylated Smad 2/3, and alpha-smooth muscle actin than lithium-treated REM sleep-deprived and control hearts. Moreover, lithium-treated REM sleep-deprived hearts had lower expression of angiotensin II type 1 receptor, phosphorylated nuclear factor kappa B p65, calcium release-activated calcium channel protein 1, transient receptor potential canonical (TRPC) 1, and TRPC3 than REM sleep-deprived hearts. The findings suggest that lithium attenuates REM sleep deprivation-induced cardiac fibrogenesis and dysfunction possibly through the downregulation of TGF-β, angiotensin II, and Ca2+ signaling. Full article
(This article belongs to the Special Issue Emerging Treatment for Cardiovascular Diseases)
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21 pages, 3864 KiB  
Article
Potential Actions of Baicalein for Preventing Vascular Calcification of Smooth Muscle Cells In Vitro and In Vivo
by Erna Sulistyowati, Jong-Hau Hsu, Szu-Jung Lee, Shang-En Huang, Widya Yanti Sihotang, Bin-Nan Wu, Zen-Kong Dai, Ming-Chung Lin and Jwu-Lai Yeh
Int. J. Mol. Sci. 2022, 23(10), 5673; https://doi.org/10.3390/ijms23105673 - 18 May 2022
Cited by 10 | Viewed by 2402
Abstract
Vascular calcification (VC) is associated with cardiovascular disease. Baicalein, a natural flavonoid extract of Scutellaria baicalensis rhizome has several biological properties which may inhibit VC. We investigated whether baicalein suppresses Runt-related transcription factor 2 (Runx2) and bone morphogenetic protein 2 (BMP-2) and upregulates [...] Read more.
Vascular calcification (VC) is associated with cardiovascular disease. Baicalein, a natural flavonoid extract of Scutellaria baicalensis rhizome has several biological properties which may inhibit VC. We investigated whether baicalein suppresses Runt-related transcription factor 2 (Runx2) and bone morphogenetic protein 2 (BMP-2) and upregulates smooth muscle 22-alpha (SM22-α) and alpha-smooth muscle actin (α-SMA). In an in vitro experiment, primary rat aortic vascular smooth muscle cells (VSMCs) were pretreated with 0.1, 1, and 5 μM baicalein, followed by β-glycerophosphate (β-GP) to induce calcification. In an in vivo experiment, VC was generated by vitamin D3 plus nicotine (VDN) administration to male Sprague Dawley (SD) rats randomly assigned into a control group, a VC group, a VC group pretreated with baicalein, and a baicalein alone group. Each group comprised 10 rats. Left ventricular (LV) morphology, function and performance were assessed by echocardiography. Calcium content was measured by Alizarin red S staining and alkaline phosphatase (ALP) activity assays. Apoptotic VSMCs were detected by flow cytometry. Protein levels and superoxide changes were evaluated using Western blotting and immunofluorescence assays respectively. Plasma malondialdehyde (MDA) was assayed. Baicalein pretreatment significantly reduced calcium content in calcified VSMCs (p < 0.001) as well as in VC rat aortic smooth muscle (p < 0.001). Additionally, ALP activity was decreased in calcified VSMCs and VC rat aortic smooth muscle (p < 0.001). Apoptosis was significantly attenuated by 1 μM baicalein pretreatment in calcified VSMCs. Runx2 and BMP-2 expressions were downregulated by the baicalein in calcified VSMCs. Baicalein pretreatment increased typical VSMCs markers SM22-α and α-SMA in calcified VSMCs. Baicalein pretreatment was associated with adverse changes in LV morphometry. Markers of oxidative stress declined, and endogenous antioxidants increased in VC rats pretreated with baicalein. Baicalein mitigates VC through the inhibition of Runx2/BMP-2 signaling pathways, enhancement of vascular contractile phenotype and oxidative stress reduction. However, our study is of basic experimental design; more advanced investigations to identify other molecular regulators of VC and their mechanisms of action is required. Full article
(This article belongs to the Special Issue Emerging Treatment for Cardiovascular Diseases)
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Review

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19 pages, 1680 KiB  
Review
Nanoparticles in the New Era of Cardiovascular Therapeutics: Challenges and Opportunities
by Pingping Yang, Jun Ren and Lifang Yang
Int. J. Mol. Sci. 2023, 24(6), 5205; https://doi.org/10.3390/ijms24065205 - 8 Mar 2023
Cited by 7 | Viewed by 2676
Abstract
Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide. Although a cadre of therapeutic strategies have been made available for CVDs in the clinical setting, predominantly through medication and surgery, these do not fully address the clinical needs of patients [...] Read more.
Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide. Although a cadre of therapeutic strategies have been made available for CVDs in the clinical setting, predominantly through medication and surgery, these do not fully address the clinical needs of patients with CVD. As a new technique for CVD treatment, nanocarriers are employed to modify and package medications to ease the targeting of tissues, cells and molecules within the cardiovascular system. Nanocarriers are made of biomaterials, metals, or a combination of these materials, with sizes similar to bioactive molecules such as proteins and DNA. Cardiovascular nanomedicine (CVN) has only surfaced in recent years and is still in its infancy. Ample studies have displayed promise for the clinical utility of nanomedicine techniques, courtesy of continued perfection in nanocarrier design to optimize drug delivery and treatment outcomes. Here in this review, we will summarize the research advances in the literature on nanoparticles in the management of CVDs, including ischemic and coronary heart disease (e.g., atherosclerosis, angina pectoris and myocardial infarction), myocardial ischemia-reperfusion injury, aortic aneurysm, myocarditis, hypertension, and pulmonary artery hypertension and thrombosis. Full article
(This article belongs to the Special Issue Emerging Treatment for Cardiovascular Diseases)
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