Background/Objectives: Numerical simulation plays an important role in pharmaceutical preparation recently. Mechanistic models, as a type of numerical model, are widely used in the study of pharmaceutical preparations. Mechanistic models are based on a priori knowledge, i.e., laws of physics, chemistry, and biology. However, due to interdisciplinary reasons, pharmacy researchers have greater difficulties in using computer models. Methods: In this paper, we highlight the application scenarios and examples of mechanistic modelling in pharmacy research and provide a reference for drug researchers to get started. Results: By establishing a suitable model and inputting preparation parameters, researchers can analyze the drug preparation process. Therefore, mechanistic models are effective tools to optimize the preparation parameters and predict potential quality problems of the product. With product quality parameters as the ultimate goal, the experiment design is optimized by mechanistic models. This process emphasizes the concept of quality by design. Conclusions: The use of numerical simulation saves experimental cost and time, and speeds up the experimental process. In pharmacy experiments, part of the physical information and the change processes are difficult to obtain, such as the mechanical phenomena during tablet compression and the airflow details in the nasal cavity. Therefore, it is necessary to predict the information and guide the formulation with the help of mechanistic models.

Cardiovascular disease (CVD) remains the leading cause of mortality worldwide, and residual inflammatory risk persists despite optimal lipid and glucose control. Emerging evidence indicates that metabolic reprogramming within immune cells constitutes a central driver of cardiovascular immune injury. In this review, we propose a unifying framework in which glyco-lipotoxicity acts as a primary metabolic trigger, inducing mitochondrial dysfunction, oxidative stress, and activation of the NLRP3 inflammasome and cGAS–STING pathways. Hyperglycaemia and dyslipidaemia reshape intracellular metabolic circuits, enhancing glycolysis and disrupting oxidative phosphorylation, thereby promoting sustained pro-inflammatory phenotypes. Crucially, metabolic intermediates function as cofactors for epigenetic remodelling. This establishes trained immunity in both circulating innate immune cells and haematopoietic stem/progenitor cells, which serves as the cellular basis for persistent metabolic memory. This persistent immunometabolic imprint amplifies sterile inflammation and accelerates vascular and myocardial remodelling. Furthermore, these processes are systemically propagated through cross-organ communication networks, including the heart–adipose, gut–heart, and cardio-hematopoietic axes, forming a multidimensional inflammatory amplification loop. We also summarise emerging therapeutic strategies targeting the metabolic–epigenetic axis, aiming to reverse maladaptive trained immunity and mitigate residual CVD risk. By integrating immunometabolism, epigenetic regulation, and organ crosstalk, this review highlights metabolic reprogramming as a pivotal mechanistic nexus and potential precision target for cardiovascular protection.

Iron (Fe), copper (Cu), and zinc (Zn) are essential trace elements for cardiovascular and cerebrovascular homeostasis, acting as enzymatic cofactors in energy metabolism and antioxidant defence. However, disruption of metal homeostasis can amplify oxidative injury through direct Fe/Cu redox chemistry or indirect Zn-dependent pathways. Ferroptosis and cuproptosis have been investigated as context-dependent mechanisms in various cardiovascular and cerebrovascular diseases (CCVDs), such as atherosclerosis, ischaemic/haemorrhagic stroke, diabetic vascular disease, and abdominal aortic aneurysm. This review summarizes the physiological regulation of metal homeostasis and examines pathways through which metal dyshomeostasis may contribute to vascular and neural injury, including oxidative biomolecular modification, mitochondrial dysfunction and inflammatory signalling. It further summarizes therapeutic strategies targeting metal metabolism, such as metal chelators, trace element supplementation and nanomedicine-based targeted delivery systems, which have shown protective effects predominantly in experimental models by restoring metal homeostasis and scavenging reactive oxygen species. Finally, the review highlights key challenges in clinical translation, such as tissue-specific metal detection and targeted inhibitor development, and emphasizes that precise regulation of metal metabolism may offer therapeutic opportunities for CCVDs.