BACKGROUND Dyslipidemia and inflammation are closely interrelated contributors in the pathogenesis of atherosclerosis. Disorders of lipid metabolism initiate an inflammatory and immune-mediated response in atherosclerosis, while low-density lipoprotein cholesterol (LDL-C) lowering has possible pleiotropic anti-inflammatory effects that extend beyond lipid lowering. MAIN TEXT Activation of the immune system/inflammasome destabilizes the plaque, which makes it vulnerable to rupture, resulting in major adverse cardiac events (MACE). The activated immune system potentially accelerates atherosclerosis, and atherosclerosis activates the immune system, creating a vicious circle. LDL-C enhances inflammation, which can be measured through multiple parameters like high-sensitivity C-reactive protein (hsCRP). However, multiple studies have shown that CRP is a marker of residual risk and not, itself, a causal factor. Recently, anti-inflammatory therapy has been shown to decelerate atherosclerosis, resulting in fewer MACE. Nevertheless, an important side effect of anti-inflammatory therapy is the potential for increased infection risk, stressing the importance of only targeting patients with high residual inflammatory risk. Multiple (auto-)inflammatory diseases are potentially related to/influenced by LDL-C through inflammasome activation. CONCLUSIONS Research suggests that LDL-C induces inflammation; inflammation is of proven importance in atherosclerotic disease progression; anti-inflammatory therapies yield promise in lowering (cardiovascular) disease risk, especially in selected patients with high (remaining) inflammatory risk; and intriguing new anti-inflammatory developments, for example, in nucleotide-binding leucine-rich repeat-containing pyrine receptor inflammasome targeting, are currently underway, including novel pathway interventions such as immune cell targeting and epigenetic interference. Long-term safety should be carefully monitored for these new strategies and cost-effectiveness carefully evaluated.

中文翻译：

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低密度脂蛋白胆固醇会引起炎症吗？如果是这样，这有关系吗？新型疗法的当前见解和未来展望。

背景技术血脂异常和炎症是动脉粥样硬化发病机理中密切相关的因素。脂质代谢紊乱会引发动脉粥样硬化的炎症反应和免疫介导的反应，而低密度脂蛋白胆固醇（LDL-C）降低则可能具有多效抗炎作用，其作用范围不仅限于脂质降低。免疫系统/炎症小体的激活破坏了斑块的稳定性，使其易于破裂，从而导致严重的不良心脏事件（MACE）。激活的免疫系统可能会加速动脉粥样硬化，而动脉粥样硬化会激活免疫系统，从而形成恶性循环。LDL-C可增强炎症，可通过多个参数（例如高敏C反应蛋白（hsCRP））进行测量。然而，多项研究表明，CRP是残留风险的标志，而本身并不是因果关系。最近，抗炎治疗已被证明可以减缓动脉粥样硬化，从而减少MACE。然而，抗炎治疗的重要副作用是可能增加感染风险，从而强调仅针对具有高残留炎性风险的患者的重要性。多种（自体）炎症性疾病可能通过炎症小体激活与LDL-C相关/受其影响。结论研究表明LDL-C可引起炎症。炎症在动脉粥样硬化疾病的进展中被证明是重要的；抗炎疗法有望降低心血管疾病的风险，特别是在某些具有较高（仍存在）炎性风险的患者中；例如，在具有核苷酸结合的富含亮氨酸的重复序列的吡喃受体炎性小体靶向方面，令人着迷的新的抗炎发展正在进行中，包括新颖的途径干预，例如免疫细胞靶向和表观遗传学干扰。对于这些新策略，应仔细监控长期安全性，并仔细评估成本效益。