2018
DOI: 10.3389/fphys.2018.01291
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The Influence of MicroRNAs on Mitochondrial Calcium

Abstract: Abnormal mitochondrial calcium ([Ca2+]m) handling and energy deficiency results in cellular dysfunction and cell death. Recent studies suggest that nuclear-encoded microRNAs (miRNA) are able to translocate in to the mitochondrial compartment, and modulate mitochondrial activities, including [Ca2+]m uptake. Apart from this subset of miRNAs, there are several miRNAs that have been reported to target genes that play a role in maintaining [Ca2+]m levels in the cytoplasm. It is imperative to validate miRNAs that al… Show more

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Cited by 20 publications
(13 citation statements)
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References 85 publications
(117 reference statements)
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“…Among them, miR-762 was demonstrated to decrease intracellular ATP levels and to increase ROS levels in cardiomyocytes [47]. Although other nuclear-encoded miRNAs may also regulate mitochondrial signaling and function [48], mitomiRs play a crucial role in post-transcriptional regulation of gene expression related to mitochondrial function (e.g., energetics and apoptosis). It is of interest to investigate the interaction of mitomiRs and other nuclear-encoded miRNAs to consummate the molecular mechanisms underlying relevant diseases in the future.…”
Section: Mitomirs and Mitochondrial Energy Metabolismmentioning
confidence: 99%
See 1 more Smart Citation
“…Among them, miR-762 was demonstrated to decrease intracellular ATP levels and to increase ROS levels in cardiomyocytes [47]. Although other nuclear-encoded miRNAs may also regulate mitochondrial signaling and function [48], mitomiRs play a crucial role in post-transcriptional regulation of gene expression related to mitochondrial function (e.g., energetics and apoptosis). It is of interest to investigate the interaction of mitomiRs and other nuclear-encoded miRNAs to consummate the molecular mechanisms underlying relevant diseases in the future.…”
Section: Mitomirs and Mitochondrial Energy Metabolismmentioning
confidence: 99%
“…AntimiR-146a treatment during pressure overload can give beneficial effects by de-repressing DLST to create a favorable metabolic profile with preserved both glucose oxidation and fatty acid oxidation in cardiomyocytes, which leads to diminished hypertrophy and an improvement in cardiac function [67]. Recently, miR-1 was found to effectively bind to the mitochondrial calcium uniporter (MCU) mRNA to influence mitochondrial Ca 2+ flux, contributing to cardiac hypertrophy [48]. In addition, miR-30 has been reported to antagonize apoptosis of cardiac cells through negatively regulating Drp1, an initiator of mitochondrial fission, Bcl-2, and Bnip3L/Nix, leading to apoptosis [55,68].…”
Section: Cardiac Hypertrophymentioning
confidence: 99%
“…Mitochondrial calcium uniport has a documented, crucial role in both proliferation and apoptosis [for reviews see e.g., ( De Stefani et al, 2015 ; Bustos et al, 2017 ; Cui et al, 2017 ; Bachmann et al, 2019 )]. The expression of the MCU subunit can be post-transcriptionally down-regulated by several small non-coding regulatory RNAs (miR), miR-25, and miR-138 ( Marchi et al, 2013 ; Hong et al, 2017 ; Jaquenod De Giusti et al, 2018 ; Figure 1 ). The miRs drastically decrease MCU protein levels, blocking thus mitochondrial Ca 2+ uptake without affecting [Ca 2+ ] C and [Ca 2+ ] ER , causing reduced apoptosis in cancer cells.…”
Section: The Mitochondrial Calcium Fluxes and Their Regulation In Celmentioning
confidence: 99%
“…In vitro and in vivo studies confirm the involvement of microRNAs in the pathogenesis of kidney diseases ( Srivastava et al, 2019a ; Metzinger-Le Meuth et al, 2019 ; Nascimento and Domingueti, 2019 ). Several microRNAs play a crucial role in mitochondria ( Gomez et al, 2013 ; Jaquenod De Giusti et al, 2018 ; Bai et al, 2019 ). MiR-30e is suppressed in renal fibrosis, and its antagonism exerts an antifibrotic effect by targeting mitochondrial protein UCP2 ( Jiang et al, 2013a ).…”
Section: Mitochondria-targetted Therapeutics In Kidney Diseasesmentioning
confidence: 99%