Studies have shown that the various parts of intestinal barrier can synergistically defend against pathogens in multiple ways.

Vitexin and isovitexin are dietary flavonoids widely distributed in food and medicinal plants. They have attracted increasing attention owing to their diverse pharmacological activities and favorable safety profiles. These compounds exhibit therapeutic potential across multiple biological systems, including the immune, nervous, respiratory, cardiovascular, and endocrine systems, through antioxidant, anti-inflammatory, anticancer, antibacterial, and neuroprotective mechanisms. Although previous reviews have addressed the pharmacological effects of vitexin and isovitexin, most are limited in scope—either focusing solely on vitexin or restricted to specific disease models such as cancer or diabetes. Moreover, some studies are outdated and do not reflect the recent advances in synthetic modification, green extraction technologies, and systems pharmacology. This review aims to provide a comprehensive evaluation of the pharmacological properties, pharmacokinetics, and clinical relevance of vitexin and isovitexin, highlighting their potential in disease prevention and treatment. A literature search was conducted using Web of Science, PubMed, and Google Scholar, with keywords including “vitexin”, “isovitexin”, “disease”, and “mechanism”. Here, we summarize the current research on the pharmacological effects of vitexin and isovitexin in metabolic disorders, inflammatory diseases, cancer, and neurodegenerative conditions, focusing on their molecular mechanisms and therapeutic targets. Furthermore, we discussed their toxicity, bioavailability, pharmacokinetics, and clinical research findings. Vitexin and isovitexin hold promise as therapeutic agents or adjuncts for multiple diseases with potential applications in modern medicine and healthcare. However, their pharmacological mechanisms, clinical efficacy, and potential synergistic effects with other therapeutic agents remain unclear. Further systematic research is needed to clarify molecular targets and optimize their therapeutic applications.

In recent years, cardiovascular diseases (CVDs) have emerged as one of the leading global risk factors for mortality. As the primary energy source for myocardial metabolism, alterations in fatty acid (FAs) metabolism play a crucial role in myocardial energy imbalance in patients with CVDs. These metabolic disruptions can affect vascular and myocardial cell function through various mechanisms, thereby contributing to the onset and progression of CVDs. Additionally, FAs are abundant in the daily diet, further emphasizing the importance of regulating FA metabolism as a potential therapeutic and preventive strategy for CVDs and its risk factors. This review systematically examines the relationship between the metabolism of short-chain, medium-chain, and long-chain FAs and CVDs, including atherosclerosis (AS), coronary heart disease (CHD), hypertension, arrhythmia, cardiomyopathy, and heart failure (HF). It also delves into the underlying mechanisms by which these FAs influence CVD pathology. Evidence suggests that short-chain FAs (SCFAs) inhibit inflammation, reduce oxidative stress, and improve endothelial function through the activation of GPR41/43 receptors. ω-3 polyunsaturated FAs (ω-3 PUFAs) reduce CVD risk by modulating lipid metabolism, inhibiting platelet aggregation, and exerting anti-inflammatory effects, whereas ω-6 PUFAs may exacerbate disease progression due to their pro-inflammatory properties. Saturated FAs (SFAs) promote CVDs by inducing lipotoxicity, oxidative stress, and vascular remodeling. Furthermore, the imbalance of key molecules in FA metabolism, such as CD36, CPT1, PPARs, and AMPK, is closely linked to myocardial energy dysfunction, inflammation, and fibrosis. This review highlights the potential of dietary interventions—such as increased intake of ω-3 PUFAs and SCFAs—as well as the targeting of FA metabolic pathways (e.g., FFARs, AMPK activators) in the prevention and treatment of CVDs. It also emphasizes the need for further clinical studies to verify the efficacy and mechanisms of these approaches. Overall, this review provides a comprehensive theoretical framework for understanding the role of FAs metabolism in CVDs and outlines directions for developing novel therapeutic strategies.