Department of Cardiology, Hippokration Hospital, 11527 Athens, Greece.
4th Department of Internal Medicine, Evangelismos Hospital, 10676 Athens, Greece.
Int J Mol Sci. 2023 Jul 22;24(14):11786. doi: 10.3390/ijms241411786.
The involvement of cardiovascular disease in cancer onset and development represents a contemporary interest in basic science. It has been recognized, from the most recent research, that metabolic syndrome-related conditions, ranging from atherosclerosis to diabetes, elicit many pathways regulating lipid metabolism and lipid signaling that are also linked to the same framework of multiple potential mechanisms for inducing cancer. Otherwise, dyslipidemia and endothelial cell dysfunction in atherosclerosis may present common or even interdependent changes, similar to oncogenic molecules elevated in many forms of cancer. However, whether endothelial cell dysfunction in atherosclerotic disease provides signals that promote the pre-clinical onset and proliferation of malignant cells is an issue that requires further understanding, even though more questions are presented with every answer. Here, we highlight the molecular mechanisms that point to a causal link between lipid metabolism and glucose homeostasis in metabolic syndrome-related atherosclerotic disease with the development of cancer. The knowledge of these breakthrough mechanisms may pave the way for the application of new therapeutic targets and for implementing interventions in clinical practice.
心血管疾病在癌症发生和发展中的作用是当前基础科学研究的热点。最近的研究已经认识到,与代谢综合征相关的疾病,从动脉粥样硬化到糖尿病,会引发许多调节脂质代谢和脂质信号的途径,这些途径也与诱导癌症的多种潜在机制相同。此外,动脉粥样硬化中的血脂异常和血管内皮细胞功能障碍可能存在共同的甚至相互依存的变化,类似于许多类型癌症中升高的致癌分子。然而,动脉粥样硬化疾病中的血管内皮细胞功能障碍是否提供了促进恶性细胞临床前发生和增殖的信号,这是一个需要进一步理解的问题,尽管每个答案都会提出更多的问题。在这里,我们强调了分子机制,这些机制表明代谢综合征相关动脉粥样硬化疾病中的脂质代谢和葡萄糖稳态与癌症的发展之间存在因果关系。对这些突破性机制的认识可能为应用新的治疗靶点和在临床实践中实施干预措施铺平道路。