Eukaryotic genomes contain a large number of transposable elements, part of which are still active and able to transpose in the host genome. Mobile element activation is repressed to avoid deleterious effects, such as gene mutations or chromosome rearrangements. Control of transposable elements includes a variety of mechanisms comprising silencing pathways, which are based on the production of small non-coding RNAs. Silencing can occur either through transposable element RNA degradation or through the targeting of DNA sequences by heterochromatin formation and consequent transcriptional inhibition. Since the important role of the heterochromatin silencing, the gradual loss of heterochromatin marks in constitutive heterochromatin regions during the aging process promotes derepression of transposable elements, which is considered a cause of the progressive increase in genomic instability and of the activation of inflammatory responses. This review provides an overview of the effects of heterochromatin loss on the activity of transposable elements during the aging process and the possible impact on genome function. In this context, we discuss the possible role of the nuclear lamina, a major player in heterochromatin dynamics, in the regulation of transposable element activity and potential implications in laminopathic diseases.

真核生物基因组包含大量转座因子，其中一部分仍然活跃并能够在宿主基因组中转座。抑制了移动元素的激活以避免有害影响，例如基因突变或染色体重排。转座因子的控制包括多种机制，这些机制包括沉默途径，这些途径基于小的非编码RNA的产生。沉默可通过转座因子RNA降解或通过异染色质形成和随后的转录抑制作用靶向DNA序列而发生。由于异染色质沉默的重要作用，在老化过程中组成性异染色质区域中异染色质标记的逐渐消失会促进转座因子的抑制，这被认为是基因组不稳定和炎症反应激活逐渐增加的原因。这篇综述概述了衰老过程中异染色质丢失对转座因子活性的影响以及对基因组功能的可能影响。在这种情况下，我们讨论了核纤层蛋白（异染色质动力学的主要参与者）在调节转座因子活性和对拉曼病的潜在影响中的可能作用。