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Abstract
Like other organs, the heart undergoes normal adaptive remodeling, such as cardiac hypertrophy, with age. This remodeling, however, is intensified under stress and pathological conditions. Cardiac remodeling could be beneficial for a short period of time, to maintain a normal cardiac output in times of need; however, chronic cardiac hypertrophy may lead to heart failure and death. MicroRNAs (miRNAs) are known to have a role in the regulation of cardiac hypertrophy. This paper reviews recent advances in the field of miRNAs and cardiac hypertrophy, highlighting the latest findings for targeted genes and involved signaling pathways. By targeting pro-hypertrophic genes and signaling pathways, some of these miRNAs alleviate cardiac hypertrophy, while others enhance it. Therefore, miRNAs represent very promising potential pharmacotherapeutic targets for the management and treatment of cardiac hypertrophy.
Highlights
The heart undergoes adaptive remodeling with age, which is exacerbated by stress and pathological stimuli, subsequently leading to cardiovascular diseases [1,2]
Because phosphatase and tensin homolog (PTEN) is a negative regulator of the autophagic phosphatidyl-3 kinase (PI3K)/AKT/mTOR cascade, it has been concluded that miR-29-associated PTEN suppression activates the PI3K/AKT/mTOR system, thereby abrogating autophagy and promoting cardiac hypertrophy [84]
A gain-of function study revealed that the hypertrophic effects of miR-23b-5p overexpression observed in the Ang-II- and transverse aortic constriction (TAC)-induced cardiac hypertrophy models was mediated via targeting high-mobility group box 2 (HMGB2) [97], a nuclear protein that regulates gene transcription, DNA recombination and repair, cell replication, and autophagy [98]
Summary
The heart undergoes adaptive remodeling with age, which is exacerbated by stress and pathological stimuli, subsequently leading to cardiovascular diseases [1,2]. Cardiac hypertrophy is a form of remodeling characterized by the enlargement of cardiomyocytes without an increase in their number. As the heart increases in size, the ventricles are enlarged, and the workload pressure on the ventricular walls decreases [1,3,4]. This helps in maintaining cardiac output efficiency under stress and pathological conditions. Based on the morphology of cardiomyocytes, cardiac hypertrophy is characterized as concentric or eccentric. 2. MMiiccrrooRRNNAAss ((mmiiRRNNAAss)) are small, non-coding RNAs approximately 20 to 22 nucleotides in length. MMiiccrrooRRNNAAss ((mmiiRRNNAAss)) are small, non-coding RNAs approximately 20 to 22 nucleotides in length They arMe vicirtoalRrNegAusla(tmoriRs NofAsse)vearrael sinmtraallc,elnlounla-rcosdigingaliRnNg Apasthawpparyosx,iwmhaitcehlym2i0ghtot e2x2plnaiunclweohtyidtehseyinare evolelnugtitohn. SomSoemmeiRmNiRANsAhsavheaavpe roatepcrtoivteecrtiovlee argoaleinastgcaainrdstiocvaarsdciuovlaarsdcuislaear sdesis,ewasheesr,eawshoetrheearss porthoemrsotpereoxmteontseive caredxitaecnrseivmeocdaerldiniagc, rleeamdoindgeltiongd,isleeaadsein. gThtoe rdeidsecaosleo.rTihnedirceadtecsomloirRiNndAiscathteast mneigRaNtiAveslythraetgnuelagtaeticvaerldyiac remreogduelalitnegc.arTdhieacgrreemenodcoellionrgi.nTdhiecagtreesemn ciRolNorAisndhiacvaitnesgmaipRoNsAitisvhearveignuglaatpoorysitriovlee.regulatory role
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