Abstract
Hypertrophic cardiomyopathy (HCM) is the most common form of hereditary cardiomyopathy. It is characterized by an unexplained non-dilated hypertrophy of the left ventricle with a conserved or elevated ejection fraction. It is a genetically heterogeneous disease largely caused by variants of genes encoding for cardiac sarcomere proteins, including MYH7, MYBPC3, ACTC1, TPM1, MYL2, MYL3, TNNI3, and TNNT23. Preclinical evidence indicates that the enhanced calcium sensitivity of the myofilaments plays a key role in the pathophysiology of HCM. Notably, this is not always a direct consequence of sarcomeric variations but may also result from secondary mutation-driven alterations. Long non-coding RNAs (lncRNAs) are a large class of transcripts ≥200 nucleotides in length that do not encode proteins. Compared to coding mRNAs, most lncRNAs are not as well-annotated and their functions are greatly unexplored. Nevertheless, increasing evidence shows that lncRNAs are involved in a variety of biological processes and diseases including HCM. Accumulating evidence has indicated that lncRNAs are dysregulated in HCM, and closely related to sarcomere construction, calcium channeling and homeostasis of mitochondria. In this review, we have summarized the known regulatory and functional roles of lncRNAs in HCM.
Highlights
Hypertrophic cardiomyopathy (HCM) is one of the most prevalent inherited disorders of cardiomyocytes, without specific geographic, ethnic, or sex patterns of distribution
Numerous studies demonstrate that Long non-coding RNAs (lncRNAs) regulate pathophysiological processes in cardiac hypertrophy by interacting with genes involved in mitochondria, sarcomeres, and calcium transition at the intracellular level (Table 3)
The pathological mation: (2) the length should be more than 200 bp: (3) it must have more than one exon mechanisms of HCM for improved treatment strategies still require further elucidation
Summary
Hypertrophic cardiomyopathy (HCM) is one of the most prevalent inherited disorders of cardiomyocytes, without specific geographic, ethnic, or sex patterns of distribution. HCM is categorized as a typical single gene disorder with variable penetrance and expression, exhibiting an autosomal dominant pattern of inheritance. HCM is characterized by an increase in the left ventricular wall thickness (end-diastolic left ventricular wall thickness ≥15 mm or the equivalent relative to the body surface area in children that cannot be solely explained by abnormal loading conditions (European Society of Cardiology Guidelines) [5]. Cardiac hypertrophy observed in HCM is typically in family members [6]. Cardiac hypertrophy observed in HCM is typically asymmetric, with the greatest involvement most commonly at the basal interventricular asymmetric, with the greatest involvement most commonly at the basal interventricular septum subjacent to the aortic valve (Figure 1A). It is infrequently restricted to other ocardial regions, such as the posterior wall of the left ventricle in symmetric hypertrophy myocardial regions, such as the posterior wall of the left ventricle in symmetric hypertrophy (Figure 1B) and at the apex in apical hypertrophy (Figure 1C)
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