The main actors of this review are Hutchinson-Gilford progeria syndrome (HGPS) and atherosclerosis.

HGPS is a very rare disease with no definitively approved specific drugs.

Atherosclerosis is a very common disease with a more consolidated treatment strategy.

Nevertheless, common mechanisms are shared by both these diseases, particularly related to inflammation, oxidative and endoplasmic reticulum (ER) stress.

Pathways regulated by Nuclear factor E2 related factor (Nrf2), Nuclear factor kappa B (NF-kB) and related to the Unfolded Protein Response (UPR) and ER stress are receiving increasing attention.

In HGPS “not omnia” happen(s) “cum tempore”, that means that HGPS patients have atherosclerotic complications before their time.

The third actor is clonal hematopoiesis: it constitutes a link between ageing and atherosclerosis.

This review aims to analyse the current knowledge of atherosclerosis and clonal hematopoiesis in order to suggest therapeutic strategies to correct the timing of the atherosclerosis progression in HGPS.

The goal for HGPS is a shift from “not omnia cum tempore” to “omnia cum tempore” in terms of significant lifespan extension by postponing atherosclerosis-related complications.

本综述的主要参与者是 Hutchinson-Gilford 早衰综合征 (HGPS) 和动脉粥样硬化。

HGPS 是一种非常罕见的疾病，没有明确批准的特定药物。

动脉粥样硬化是一种非常常见的疾病，治疗策略更为统一。

尽管如此，这两种疾病都有共同的机制，特别是与炎症、氧化和内质网 (ER) 应激有关。

受核因子 E2 相关因子 ( Nrf2 )、核因子 kappa B ( NF-kB )调控的通路以及与未折叠蛋白反应 (UPR) 和内质网应激相关的通路正受到越来越多的关注。

在 HGPS 中“not omnia”发生“cum tempore”，这意味着 HGPS 患者在他们的时间之前就有动脉粥样硬化并发症。

第三个因素是克隆造血：它构成了衰老和动脉粥样硬化之间的联系。

本综述旨在分析目前对动脉粥样硬化和克隆造血的认识，以提出治疗策略，以纠正 HGPS 中动脉粥样硬化进展的时间。

HGPS 的目标是通过推迟与动脉粥样硬化相关的并发症，在显着延长寿命方面从“非全神贯注”转变为“全神贯注”。