MicroRNAs and Calcium Signaling in Heart Disease

Park, Jae-Ho; Kho, Changwon

doi:10.3390/ijms221910582

Cited by 17 publications

(9 citation statements)

References 109 publications

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“…In the study by Muraoka et al [ 48 ], miR-133 overexpression inhibited the expression of numerous genes in fibroblasts, also activating the cardiac gene program. MiR-1 downregulation was reported in failing hearts, in the tissues of patients with dilated cardiomyopathy and aortic stenosis and in hearts with ischemic cardiomyopathy [ 49 ]. Of note, miR-1 is expressed in cardiac fibroblasts, which are among the major non-muscle cell types in the myocardium and are responsible for cardiac fibrosis under pathological conditions.…”

Section: Discussionmentioning

confidence: 99%

MiRNA-Mediated Fibrosis in the Out-of-Target Heart following Partial-Body Irradiation

Tanno

Novelli

Leonardi

et al. 2022

Cancers

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Recent reports have shown a link between radiation exposure and non-cancer diseases such as radiation-induced heart disease (RIHD). Radiation exposures are often inhomogeneous, and out-of-target effects have been studied in terms of cancer risk, but very few studies have been carried out for non-cancer diseases. Here, the role of miRNAs in the pathogenesis of RIHD was investigated. C57Bl/6J female mice were whole- (WBI) or partial-body-irradiated (PBI) with 2 Gy of X-rays or sham-irradiated (SI). In PBI exposure, the lower third of the mouse body was irradiated, while the upper two-thirds were shielded. From all groups, hearts were collected 15 days or 6 months post-irradiation. The MiRNome analysis at 15 days post-irradiation showed that miRNAs, belonging to the myomiR family, were highly differentially expressed in WBI and PBI mouse hearts compared with SI hearts. Raman spectral data collected 15 days and 6 months post-irradiation showed biochemical differences among SI, WBI and PBI mouse hearts. Fibrosis in WBI and PBI mouse hearts, indicated by the increased deposition of collagen and the overexpression of genes involved in myofibroblast activation, was found 6 months post-irradiation. Using an in vitro co-culture system, involving directly irradiated skeletal muscle and unirradiated ventricular cardiac human cells, we propose the role of miR-1/133a as mediators of the abscopal response, suggesting that miRNA-based strategies could be relevant for limiting tissue-dependent reactions in non-directly irradiated tissues.

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Section: Discussionmentioning

confidence: 99%

MiRNA-Mediated Fibrosis in the Out-of-Target Heart following Partial-Body Irradiation

Tanno

Novelli

Leonardi

et al. 2022

Cancers

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“…In aged cardiomyocytes, impaired Ca 2+ handling results from age-related modification in proteins associated with the ECC [121][122][123]. The expression levels of SERCA2a decreased with aging and seems to be the primary mechanisms for the extended Ca 2+ transients [124].…”

Section: Calcium Signaling Impairmentsmentioning

confidence: 99%

Cardiac System during the Aging Process

Ribeiro¹,

Zerolo²,

López-Espuela³

et al. 2023

Aging and disease

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The aging process is accompanied by a continuous decline of the cardiac system, disrupting the homeostatic regulation of cells, organs, and systems. Aging increases the prevalence of cardiovascular diseases, thus heart failure and mortality. Understanding the cardiac aging process is of pivotal importance once it allows us to design strategies to prevent age-related cardiac events and increasing the quality of live in the elderly. In this review we provide an overview of the cardiac aging process focus on the following topics: cardiac structural and functional modifications; cellular mechanisms of cardiac dysfunction in the aging; genetics and epigenetics in the development of cardiac diseases; and aging heart and response to the exercise.

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“…Moreover, given the therapeutic implications of targeting Ca 2+ cycling, in-depth studies of specific miRNAs that regulate Ca 2+ mishandling in DMD are warranted. In particular, research on miRNAs that regulate calcium metabolism in heart disease is being actively conducted [ 100 ].…”

Section: Micrornas With Therapeutic Potentialmentioning

confidence: 99%

MicroRNAs in Dystrophinopathy

Lee

Moon²,

Yü³

et al. 2022

IJMS

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Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD), which represent the range of dystrophinopathies, account for nearly 80% of muscle dystrophy. DMD and BMD result from the loss of a functional dystrophin protein, and the leading cause of death in these patients is cardiac remodeling and heart failure. The pathogenesis and progression of the more severe form of DMD have been extensively studied and are controlled by many determinants, including microRNAs (miRNAs). The regulatory role of miRNAs in muscle function and the differential miRNA expression in muscular dystrophy indicate the clinical significance of miRNAs. This review discusses the relevant microRNAs as potential biomarkers and therapeutic targets for DMD and DMD cardiomyopathy as examples of dystrophinopathies.

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MicroRNAs and Calcium Signaling in Heart Disease

Cited by 17 publications

References 109 publications

MiRNA-Mediated Fibrosis in the Out-of-Target Heart following Partial-Body Irradiation

MiRNA-Mediated Fibrosis in the Out-of-Target Heart following Partial-Body Irradiation

Cardiac System during the Aging Process

MicroRNAs in Dystrophinopathy

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