Molecular and Cellular Mechanisms in Anti-Thrombosis

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 28 February 2025 | Viewed by 647

Special Issue Editors


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Guest Editor
Department of Pharmacology, Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan
Interests: cardiovascular pharmacology; protein bio—chemistry; signal transduction; platelet biology; anti-thrombotic drug development
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Guest Editor
Department of Ecology and Environmental Sciences, School of Life Sciences, Pondicherry University, Puducherry, India
Interests: natural product chemistry; oxidative stress/antioxidant research; environmental toxicology; molecular phytotherapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cerebrovascular disease is one of the biggest health problems across the globe. Both large and minor cerebral vascular diseases have the potential to cause stroke and to exacerbate the vascular component of other types of neurological disorders. Even while neurovascular illness and the damage that follows ischemia episodes are important, our understanding of neuroprotection and vascular biology in general is still lacking in these areas. Based on the available epidemiological data, coronary heart disease and cerebral hemorrhage were predicted to be the leading causes of mortality for people up to the year 2020. Nevertheless, despite a number of advancements that have aided in our knowledge of illnesses, conventional medicine's use of pharmaceuticals to treat them has not produced satisfying outcomes.

Numerous studies have demonstrated the effectiveness of medication-assisted management of traditional risk factors in lowering cardiovascular events. In addition to using pharmaceuticals to treat cardiovascular risk factors and antithrombotic medications, more people are becoming aware of the potential therapeutic applications of herbal remedies and other natural products as well as their function in the prevention of vascular disorders. Research on the effects of the main risk factors for thrombotic and cerebrovascular illness may open up new avenues for preventing ischemic episodes and enhancing the prognosis of existing patients. Because macrophages and microglia may be important regulators of the blood–brain barrier following stroke. As a result, the goal of this Special Issue was to encourage participation through both original and review papers that would spark long-term efforts to comprehend the pathophysiology behind cerebral–neuro-vascular disorders and to expand on treatment and prevention techniques.

Prof. Dr. Joen-Rong Sheu
Dr. Thanasekaran Jayakumar
Guest Editors

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Keywords

  • platelet activation and thrombosis
  • neuroprotection
  • antithrombotic mechanisms

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Published Papers (1 paper)

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Research

17 pages, 6574 KiB  
Article
Glabridin Suppresses Macrophage Activation by Lipoteichoic Acid In Vitro: The Crucial Role of MAPKs-IL-1β-iNOS Axis Signals in Peritoneal and Alveolar Macrophages
by Shaw-Min Hou, Chun-Ming Yang, Wei-Chieh Huang, Ssu-Wei Cheng, Ting-Lin Yen, Chih-Wei Hsia, Cheng-Ying Hsieh and Chih-Hsuan Hsia
Biomolecules 2025, 15(2), 174; https://doi.org/10.3390/biom15020174 - 24 Jan 2025
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Abstract
Inflammation, a fundamental response to infection and injury, involves interactions among immune cells and signaling molecules. Dysregulated inflammation contributes to diseases such as autoimmune disorders and cancer. Interleukin-1 beta (IL-1β), produced by macrophages in response to lipoteichoic acid (LTA) from Gram-positive bacteria, is [...] Read more.
Inflammation, a fundamental response to infection and injury, involves interactions among immune cells and signaling molecules. Dysregulated inflammation contributes to diseases such as autoimmune disorders and cancer. Interleukin-1 beta (IL-1β), produced by macrophages in response to lipoteichoic acid (LTA) from Gram-positive bacteria, is a key inflammatory mediator. Glabridin (GBD), a bioactive compound from licorice root, exhibits anti-inflammatory properties. This study investigates GBD’s effects on LTA-induced proinflammatory signaling in RAW 264.7 murine macrophages and alveolar macrophages, MH-S, focusing on IL-1β expression and signaling pathways. Cell viability assays confirmed that 20 μM GBD was non-cytotoxic. Confocal microscopy and quantitative PCR showed that GBD significantly reduced IL-1β fluorescence intensity, mRNA, and protein levels. GBD also inhibited inducible nitric oxide synthase (iNOS) expression and nitric oxide (NO) production. Further analysis revealed that GBD suppressed NF-κB p65 nuclear translocation and selectively modulated MAPK pathway activation by reducing JNK and p38 MAPK phosphorylation without affecting ERK. Studies using specific inhibitors demonstrated that IL-1β production reduction was mechanistically linked to MAPK pathway inhibition. These findings highlight GBD’s potential as a therapeutic agent for inflammatory diseases through its ability to modulate critical inflammatory mediators and signaling pathways. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms in Anti-Thrombosis)
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