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Cardiovascular Diseases: Molecular Mechanism and Therapeutic Strategies

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: 30 June 2025 | Viewed by 210

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Special Issue Information

Dear Colleagues,

This Special Issue delves into the intersection of molecular biology and therapeutic innovations in cardiovascular diseases (CVDs), emphasizing the intricate mechanisms driving heart and blood vessel disorders and their potential treatments. The title comprehensively explores the fundamental cellular processes contributing to cardiovascular dysfunction and the cutting-edge strategies to address these conditions.

The focus on "molecular mechanisms" underscores an in-depth investigation into how CVDs develop at the cellular and genetic levels. Key areas include inflammation, oxidative stress, apoptosis, and vascular remodeling pathways. Understanding these processes is critical for uncovering novel therapeutic targets and advancing the development of more effective treatments.

The "therapeutic strategies" aspect highlights the application of molecular insights to medical practice, encompassing established therapies and emerging approaches such as gene therapy, targeted pharmacological interventions, and personalized medicine. This integration of molecular research and clinical innovation represents a modern, holistic approach to cardiovascular medicine, where discoveries at the bench are seamlessly translated to bedside applications.

This Special Issue is poised to serve as a vital resource for cardiovascular medicine researchers, clinicians, and pharmaceutical developers. It will offer valuable perspectives on disease mechanisms and pioneering treatment strategies.

Prof. Dr. Tzong-Shyuan Lee
Guest Editor

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Keywords

  • cardiovascular diseases
  • vascular
  • atherosclerosis
  • heart failure
  • stroke
  • oxidative stress
  • personalized medicine

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Published Papers (1 paper)

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Research

17 pages, 2733 KiB  
Article
HMGB1 Regulates Adipocyte Lipolysis via Caveolin-1 Signaling: Implications for Metabolic and Cardiovascular Diseases
by Julia Chu-Ning Hsu, Kuan-Ting Chiu, Chia-Hui Chen, Chih-Hsien Wang, Song-Kun Shyue and Tzong-Shyuan Lee
Int. J. Mol. Sci. 2025, 26(9), 4222; https://doi.org/10.3390/ijms26094222 - 29 Apr 2025
Abstract
High-mobility group box 1 (HMGB1) is a nuclear protein that can be secreted or released into the extracellular environment during cellular stress, functioning as a damage-associated molecular pattern molecule. This study investigates the role of HMGB1 in adipocyte development and metabolism, explicitly examining [...] Read more.
High-mobility group box 1 (HMGB1) is a nuclear protein that can be secreted or released into the extracellular environment during cellular stress, functioning as a damage-associated molecular pattern molecule. This study investigates the role of HMGB1 in adipocyte development and metabolism, explicitly examining its interaction with β3-adrenergic receptor-mediated lipolysis and caveolin-1 (CAV1) regulation, which may influence cardiovascular risk factors. Using 3T3-L1 preadipocytes and mouse embryonic fibroblasts, we demonstrated that HMGB1 expression increases progressively during adipogenesis, reaching peak levels in mature adipocytes. While exogenous HMGB1 treatment did not affect preadipocyte proliferation or differentiation, it inhibited lipolysis in mature adipocytes. Mechanistically, HMGB1 suppressed β3-adrenergic receptor agonist CL-316,243-induced hormone-sensitive lipase activation by reducing protein kinase A-mediated phosphorylation and attenuating extracellular signal-regulated kinase signaling without affecting upstream cyclic AMP levels. We discovered a novel regulatory mechanism wherein CAV1 physically interacts with HMGB1 in mature adipocytes, with c-Src-dependent CAV1 phosphorylation functioning as a negative regulator of HMGB1 secretion. This finding was confirmed in CAV1-deficient models, which displayed increased HMGB1 secretion and diminished lipolytic activity both in vitro and in vivo. Furthermore, administering HMGB1-neutralizing antibodies to wild-type mice enhanced fasting-induced lipolysis, establishing circulating HMGB1 as a crucial antilipolytic factor. These findings reveal HMGB1’s previously uncharacterized role in adipose tissue metabolism as a negative regulator of lipolysis through CAV1-dependent mechanisms. This work provides new insights into adipose tissue metabolism regulation and identifies potential therapeutic targets for obesity-related metabolic disorders and cardiovascular diseases. Full article
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