E-cigarettes have surged in popularity in the last decade. While they are generally viewed as a safe alternative to smoking tobacco, studies suggest that E-cigarettes, like tobacco ones, cause oxidative stress, inflammation and endothelial dysfunction in users. Indeed, the aerosols produced during vaping contain comparable levels of reactive oxygen species (ROS) to those in tobacco smoke. Data on the extent to which E-cigarette ROS influence cardiovascular health is lacking, however. To address this, Gupta and colleagues recruited 32 chronic users of E-cigarettes, 29 chronic tobacco smokers, and 45 individuals that used neither, and measured their plasma levels of oxidative biomarkers. The team found similarities and differences between E-cigarette and tobacco users. Both, for example, had increased plasma antioxidant capacity and decreased levels of oxidized linoleic acid compared with the levels seen in non-users, while arachidonic acid levels were raised in tobacco smokers and reduced in the E-cigarette users. Overall, however, biomarker levels were deemed to be intermediate for E-cigarette users between non-users and tobacco users. The study suggests, therefore, that while E-cigarettes carry a lower health risk than tobacco ones, they are by no means safe.

Diabetes, high blood pressure and obesity are risk factors for both cardiovascular disease (CVD) and chronic kidney disease (CKD). Worse still, loss of kidney function and even dialysis itself are thought to exacerbate cardiovascular issues. In the case of dialysis, it’s thought that high levels of glucose degradation products (GDPs) in the dialysis fluids can promote the addition of sugar moieties to vascular proteins and lipids (glycation), causing vessel damage. To investigate this theory, Bartosova and colleagues studied vascular tissue from children with CKD receiving dialysis fluid with either high levels or low levels of GDPs, or that were not on dialysis at all. Proteome and transcriptome analyses of the vessel tissues revealed that, compared with patients on no or low-GDP fluids, patients receiving high-GDP fluids had higher levels of damaging glycation, increased transcription of genes involved in cell death, and decreased transcription of genes involved in cell survival and cytoskeleton organization. In line with these findings, vessels from high-GDP patients displayed considerable evidence of damage (apoptosis, cytoskeletal disintergration, thickened intimas). The results thus confirm GDPs can cause vasculopathy and suggest low-GDP fluids should be favored for dialysis.

While excess lipids in the blood spur the development of atherosclerosis, the disease quickly becomes one of chronic inflammation that encourages the persistence of the lipid-filled plaques in vessel walls. Indeed, sustained inflammation is thought to explain why lipid-lowering drugs often aren’t enough to combat the condition. Inflammation-suppressing drugs are also being investigated, but because these may cause susceptibility to infections, Schlegel and colleagues reasoned that promoting resolution of inflammation may be a preferable goal. To that end, the team tested blocking nectrin-1 in atherosclerosis-prone mice. Originally identified as a factor essential for nerve cells, Netrin-1 has also been found in macrophages where it promotes persistence and survival of the cells in atherosclerotic plaques. The team showed that in mice with advanced atherosclerosis, turning off netrin-1 in macrophages—via an inducible genetic switch—led to significant plaque regression. Not only did plaque macrophages exhibit reduced retention, proliferation and survival, those that remained were more likely to be pro-resolving. While susceptibility to infection was not investigated in this study, the results suggest in principle that netrin-1 blockade could be a strategy for atherosclerosis treatment.

电子烟在过去十年中大受欢迎。虽然它们通常被视为吸烟的安全替代品，但研究表明，电子烟与烟草一样，会导致使用者的氧化应激、炎症和内皮功能障碍。事实上，电子烟过程中产生的气溶胶含有与烟草烟雾中的活性氧 (ROS) 水平相当的活性氧 (ROS)。然而，缺乏关于电子烟 ROS 影响心血管健康程度的数据。为了解决这个问题，Gupta 及其同事招募了 32 名长期吸电子烟者、29 名长期吸烟者和 45 名两者都不使用的人，并测量了他们的血浆氧化生物标志物水平。该团队发现了电子烟和烟草使用者之间的异同。两者，例如，与非吸食者相比，其血浆抗氧化能力增加，氧化亚油酸水平降低，而吸烟者的花生四烯酸水平升高，而电子烟使用者的花生四烯酸水平降低。然而，总体而言，生物标志物水平被认为是电子烟使用者在非使用者和烟草使用者之间的中间水平。因此，该研究表明，虽然电子烟的健康风险低于烟草，但它们绝不安全。

糖尿病、高血压和肥胖是心血管疾病 (CVD) 和慢性肾病 (CKD) 的危险因素。更糟糕的是，肾功能丧失甚至透析本身被认为会加剧心血管问题。在透析的情况下，人们认为透析液中高水平的葡萄糖降解产物 (GDP) 会促进糖部分添加到血管蛋白质和脂质中（糖化），从而导致血管损伤。为了研究这一理论，Bartosova 及其同事研究了 CKD 儿童的血管组织，这些儿童接受了高水平或低水平 GDP 的透析液，或者根本没有进行透析。血管组织的蛋白质组和转录组分析表明，与没有或低 GDP 液体的患者相比，接受高 GDP 液体的患者具有更高水平的破坏性糖基化，参与细胞死亡的基因转录增加，以及参与细胞存活和细胞骨架组织的基因转录减少。与这些发现一致，来自高 GDP 患者的血管显示出相当多的损伤证据（细胞凋亡、细胞骨架解体、内膜增厚）。因此，结果证实 GDP 会导致血管病变，并表明应该倾向于使用低 GDP 液体进行透析。

虽然血液中过多的脂质会刺激动脉粥样硬化的发展，但这种疾病很快就会成为一种慢性炎症，促使血管壁中充满脂质的斑块持续存在。事实上，持续的炎症被认为可以解释为什么降脂药物通常不足以对抗这种疾病。炎症抑制药物也正在研究中，但由于这些药物可能导致易感染，Schlegel 及其同事推断，促进炎症消退可能是一个更可取的目标。为此，该团队在易患动脉粥样硬化的小鼠中测试了阻断 necrin-1。Netrin-1 最初被确定为神经细胞必需的因子，但在巨噬细胞中也被发现，它促进动脉粥样硬化斑块中细胞的持久性和存活。研究小组表明，在患有晚期动脉粥样硬化的小鼠中，通过诱导型基因开关关闭巨噬细胞中的 netrin-1 导致显着的斑块消退。不仅斑块巨噬细胞表现出减少的保留、增殖和存活，那些留下的更有可能是促消退的。虽然本研究未调查对感染的易感性，但结果原则上表明，netrin-1 阻断可能是动脉粥样硬化治疗的一种策略。