New Advances in Cardiovascular Drugs: In Memory of Professor Akira Endo

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Drug Discovery, Development and Delivery".

Deadline for manuscript submissions: closed (30 April 2025) | Viewed by 1118

Special Issue Editor

Special Issue Information

Dear Colleagues,

We dedicate this Special Issue in celebration of the 90th birthday of Prof. Akira Endo, an internationally renowned Japanese biochemist whose research into the relationship between fungi and cholesterol biosynthesis led to the development of the first statin (ML-236B; compactin) 50 years ago, providing a relevant contribution to the advance of cardiovascular pharmacology.

Prof. Akira Endo (born 14 November 1933, in Higashiyuri, Northern Japan) developed an interest in fungi since young age, being an admirer of Alexander Fleming. He degreed from the Faculty of Agriculture at Tokohu University in 1957 and started working as a research fellow in the pharmaceutical company Sankyo, in Tokyo. His research focused on fungal enzymes for processing fruit juice, and, due to successful discoveries in the field, moved to New York after receiving his PhD from the Tokohu University in 1966. In New York, he spent 2 years as a research associate at the Albert Einstein College of Medicine and worked on cholesterol, before returning to Sankyo’s research laboratories in 1968. It was here that Prof. Endo speculated that some fungi might produce antibiotics to inhibit the enzyme responsible for the rate-limiting step in cholesterol synthesis, 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase, possibly as a defence mechanism against other microbes. Prof. Endo started his exploratory research in April 1971, analysing about 6000 compounds, and discovered the first statin mevastatin (ML-236B; compactin) in 1973. The wind of change that would have brought such a discovery was not yet known. In fact, at that time, little was known about low-density lipoprotein (LDL) regulation mechanisms since Brown and Goldstein only began their studies that would have led to the discovery of LDL receptor in 1972. As statin research gained attention, other pharmaceutical companies joined in and, in 1978, Merck isolated a compactin-like substance from Aspergillus terreus, whilst, simultaneously, the same compound was discovered by Prof. Endo from Monascus ruber, and lovastatin was born. It took over 10 years preclinical and clinical trials before the approval and commercialization of lovastatin that occurred in 1987 in USA, also paving the way for further statin drugs development.

Prof. Endo became an associate professor in the late 1970s and in 1986 a full professor at Tokyo University of Agriculture and Technology, where he enlightened the minds of young researchers until his retirement. After his official retirement, he became the president of Biopharm Research Laboratories. Thanks to Prof. Endo’s perseverance and enthusiasm in deepening his research, statins are now used to prevent cardiovascular events globally, as well as improving the quality of life of patients.

In this commemorative Special Issue, the scope of which is to detail the advances in cardiovascular drugs in the last few decades, we welcome scientific contributions with the aim of gathering accurate and up-to-date scientific information on laboratory studies of new and upcoming treatment opportunities for cardiovascular diseases. It is my privilege to invite you and your co-workers to share their experience and expertise by submitting original research articles, systematic reviews, and review articles reporting new ideas and recent advances related to this topic.

Dr. Alfredo Caturano
Guest Editor

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Keywords

  • cardiovascular drugs
  • statins
  • metformin
  • SGLT2i
  • laboratory
  • drug targets
  • translational research
  • targeted therapy

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23 pages, 1705 KiB  
Review
Lysosomal Stress in Cardiovascular Diseases: Therapeutic Potential of Cardiovascular Drugs and Future Directions
by Toshiki Otoda, Ken-ichi Aihara and Tadateru Takayama
Biomedicines 2025, 13(5), 1053; https://doi.org/10.3390/biomedicines13051053 - 27 Apr 2025
Viewed by 427
Abstract
Lysosomal dysfunction has emerged as a central contributor to the pathogenesis of cardiovascular diseases (CVDs), particularly due to its involvement in chronic inflammation, lipid dysregulation, and oxidative stress. This review highlights the multifaceted roles of lysosomes in CVD pathophysiology, focusing on key mechanisms [...] Read more.
Lysosomal dysfunction has emerged as a central contributor to the pathogenesis of cardiovascular diseases (CVDs), particularly due to its involvement in chronic inflammation, lipid dysregulation, and oxidative stress. This review highlights the multifaceted roles of lysosomes in CVD pathophysiology, focusing on key mechanisms such as NLRP3 inflammasome activation, TFEB-mediated autophagy regulation, ferroptosis, and the role of apolipoprotein M (ApoM) in preserving lysosomal integrity. Additionally, we discuss how impaired lysosomal acidification, mediated by V-ATPase, contributes to lipid-induced cardiac dysfunction. Therapeutically, several pharmacological agents, such as statins, SGLT2 inhibitors, TRPML1 agonists, resveratrol, curcumin, and ferroptosis modulators (e.g., GLS1 activators and icariin), have demonstrated promise in restoring lysosomal function, enhancing autophagic flux, and reducing inflammatory and oxidative injury in both experimental models and early clinical settings. However, key challenges remain, including limitations in drug delivery systems, the absence of lysosome-specific biomarkers, and insufficient clinical validation of these strategies. Future research should prioritize the development of reliable diagnostic tools for lysosomal dysfunction, the optimization of targeted drug delivery, and large-scale clinical trials to validate therapeutic efficacy. Incorporating lysosome-modulating approaches into standard cardiovascular care may offer a new precision medicine paradigm for managing CVD progression. Full article
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