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EDITORIAL article

Front. Pharmacol.
Sec. Cardiovascular and Smooth Muscle Pharmacology
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1566159
This article is part of the Research Topic Reviews in Cardiovascular Pharmacology: 2023 View all 13 articles

Editorial: Reviews in Cardiovascular Pharmacology: 2023

Provisionally accepted
  • 1 Faculty of Medicine Universiti Kebangaan Malaysia, Kuala Lumpur, Malaysia
  • 2 Faculty of Medicine, Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia
  • 3 University of British Columbia, Vancouver, British Columbia, Canada
  • 4 Faculty of Medicine, Universitas Padjajaran, Bandung, Indonesia

The final, formatted version of the article will be published soon.

    Cardiovascular diseases remains a leading cause of death globally, accounting for approximately 17.9 million fatalities in 2019 (WHO, 2021). Cardiovascular diseases include hypertension, atherosclerosis, ischemic heart disease, stroke and heart failure, and imposes a significant socioeconomic burden. The Research Topic "Reviews in Cardiovascular Pharmacology: 2023" provides an overview of both the pathogenesis and pharmacological advances in cardiovascular diseases. This collection features twelve articles, each offering in-depth discussions on recent findings on the mechanisms underlying cardiovascular diseases, as well as the development and application of novel cardiovascular therapies. The articles cover a wide range of topics, including recent advancements in clinical trials, emerging concepts on drug mechanisms, therapeutic strategies, and challenges related to pharmacokinetics.Nitric oxide (NO) is a highly reactive gaseous molecule released by endothelial cells in blood vessels, playing a crucial role in mediating protective cardiovascular effects, including vasodilation (Siti et al., 2019). Impaired NO function often occurs before the clinical onset of cardiovascular disease (). This endogenous vasodilator binds to soluble guanylate cyclase (sGC), stimulating the synthesis of cyclic guanosine monophosphate (cGMP). Elevated cGMP activates protein kinase G (PKG), which lowers intracellular calcium levels in vascular smooth muscle cells, inducing vasodilation (Mishra et al., 2025). Yin et al. review the progress of guanylate cyclase activators to stimulate the NO-sGC-cGMP signaling pathway in patients with cardiovascular disease. These include riociguat,vericiguat,praliciguat,olinciguat,cinaciguat,ataciguat,runcaciguat,mosliciguat,and BI 685509,the The authors declare that the editorial was written in the absence of any commercial or financial 117 relationships that could be construed as a potential conflict of interest. 118

    Keywords: Cardiac, vascular, Fibrosis, Atherosclerosis, Inflammation, Oxidative Stress

    Received: 24 Jan 2025; Accepted: 31 Jan 2025.

    Copyright: © 2025 Kamisah, Laher and Syamsunarno. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Yusof Kamisah, Faculty of Medicine Universiti Kebangaan Malaysia, Kuala Lumpur, Malaysia

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.