The heart is the first organ to form and undergoes adaptive remodelling with age. Ventricular hypertrophy is one such adaptation, which allows the heart to cope with an increase in cardiac demand. This adaptation is necessary as part of natural growth from foetal life to adulthood. It may also occur in response to resistance in blood flow due to various insults on the heart and vessels that accumulate with age. The heart can only compensate to this increase in workload to a certain extent without losing its functional architecture, ultimately resulting in heart failure. Many genes have been implicated in cardiac hypertrophy, however none have been shown conclusively to be responsible for pathological cardiac hypertrophy. MicroRNAs offer an alternative mechanism for cellular regulation by altering gene expression. Since 1993 when the function of a non‐coding DNA sequence was first discovered in the model organism Caenorhabditis elegans, many microRNAs have been implicated in having a central role in numerous physiological and pathological cellular processes. The level of control these antisense oligonucleotides offer can often be exploited to manipulate the expression of target genes. Moreover, altered levels of microRNAs can serve as diagnostic biomarkers, with the prospect of diagnosing a disease process as early as during foetal life. Therefore, it is vital to ascertain and investigate the function of microRNAs that are involved in heart development and subsequent ventricular remodelling. Here we present an overview of the complicated network of microRNAs and their target genes that have previously been implicated in cardiogenesis and hypertrophy. It is interesting to note that microRNAs in both of these growth processes can be of possible remedial value to counter a similar disease pathophysiology.

中文翻译：

---

肥厚心脏中的微小RNA：从胎儿到成年

心脏是第一个形成的器官，随着年龄的增长会发生适应性重塑。心室肥大就是这样一种适应，它使心脏能够应对心脏需求的增加。作为从胎儿到成年的自然成长的一部分，这种适应是必要的。它也可能是由于随着年龄增长而对心脏和血管造成的各种损伤引起的血流阻力的反应。心脏只能在一定程度上补偿这种增加的工作量，而不会失去其功能架构，最终导致心力衰竭。许多基因都与心脏肥大有关，但是没有一个基因最终被证明与病理性心脏肥大有关。MicroRNAs 通过改变基因表达为细胞调控提供了一种替代机制。自 1993 年首次在模型生物秀丽隐杆线虫中发现非编码 DNA 序列的功能以来，许多 microRNA 在许多生理和病理细胞过程中发挥着核心作用。这些反义寡核苷酸提供的控制水平通常可用于操纵目标基因的表达。此外，改变水平的 microRNA 可以作为诊断生物标志物，有望早在胎儿时期就诊断出疾病过程。因此，确定和研究参与心脏发育和随后心室重构的 microRNA 的功能至关重要。在这里，我们概述了以前与心脏发生和肥大有关的 microRNA 及其靶基因的复杂网络。