Cellular senescence, a process that induces irreversible cell cycle arrest in response to diverse stressors, is a primary contributor to aging and age-related diseases. Currently, exposure to hydrogen peroxide is a widely used technique for establishing in vitro cellular senescence models; however, this traditional method is inconsistent, laborious, and ineffective in vivo. To overcome these limitations, we have developed a hydrogen peroxide-releasing hydrogel that can readily and controllably induce senescence in conventional 2-dimensional cell cultures as well as advanced 3-dimensional microphysiological systems. Notably, we have established 2 platforms using our hydrogen peroxide-releasing hydrogel for investigating senolytics, which is a promising innovation in anti-geronic therapy. Conclusively, our advanced model presents a highly promising tool that offers a simple, versatile, convenient, effective, and highly adaptable technique for inducing cellular senescence. This innovation not only lays a crucial foundation for future research on aging but also markedly accelerates the development of novel therapeutic strategies targeting age-related diseases.

Tuan Anh Vuong, Yan Zhang, June Kim, Young-Eun Leem & Jong-Sun Kang. BMB Reports 2024;57:330-5. https://doi.org/10.5483/BMBRep.2023-0203

Cardiovascular diseases (CVDs) and metabolic disorders stand as formidable challenges that significantly impact the clinical outcomes and living quality for afflicted individuals. An intricate comprehension of the underlying mechanisms is paramount for the development of efficacious therapeutic strategies. Protein arginine methyltransferases (PRMTs), a class of enzymes responsible for the precise regulation of protein methylation, have ascended to pivotal roles and emerged as crucial regulators within the intrinsic pathophysiology of these diseases. Herein, we review recent advancements in research elucidating on the multifaceted involvements of PRMTs in cardiovascular system and metabolic diseases, contributing significantly to deepen our understanding of the pathogenesis and progression of these maladies. In addition, this review provides a comprehensive analysis to unveil the distinctive roles of PRMTs across diverse cell types implicated in cardiovascular and metabolic disorders, which holds great potential to reveal novel therapeutic interventions targeting PRMTs, thus presenting promising perspectives to effectively address the substantial global burden imposed by CVDs and metabolic disorders.

Shibo Wei, Yan Zhang, Baeki E. Kang, Wonyoung Park, He Guo, Seungyoon Nam, Jong-Sun Kang, Jee-Heon Jeong, Yunju Jo, Dongryeol Ryu, Yikun Jiang & Ki-Tae Ha. BMB Reports 2024;57:287-92. https://doi.org/10.5483/BMBRep.2023-0214

Glycolysis is a defining feature of cancer metabolism, originally described by the Warburg effect. Increasing evidence indicates that cancer-associated glycolysis is not uniformly upregulated but dynamically rewired in response to oncogenic signaling, cellular demands, and microenvironmental cues. However, a framework integrating its temporal evolution and functional roles across tumorigenesis remains limited. In particular, how glycolytic rewiring drives malignant transformation, adapts during tumor progression, and generates context-dependent vulnerabilities has not been systematically synthesized. In this review, we examine glycolysis as a dynamic metabolic network evolving throughout tumor development. We discuss how early glycolytic rewiring, driven by oncogenic signaling and metabolic–epigenetic coupling, supports cell fate transitions and establishes redox and biosynthetic capacity during tumorigenesis. We then outline how glycolysis is remodeled during tumor progression through coordinated transcriptional, epigenetic, and post-translational regulation, as well as microenvironmental interactions and metabolic heterogeneity. Furthermore, we highlight glycolysis as an integrative hub linking immune evasion, cell death regulation, and metabolic plasticity, and discuss how glycolytic rewiring creates context-dependent metabolic dependencies that may be therapeutically exploited, along with emerging technologies that enable high-resolution characterization of tumor metabolism. Together, this review provides a conceptual framework for understanding glycolytic rewiring in cancer and outlines potential avenues for targeting metabolic vulnerabilities.