MicroRNA-136-5p protects cardiomyocytes from coronary microembolization through the inhibition of pyroptosis

Cai, Ruping; Xu, Yu; Ren, Yi; He, Shirong; Zheng, Jing; Kong, Biao; Li, Quanzhong; Yang, Xiheng; Dai, Rixin; Wei, Riming; Su, Qiang

doi:10.1007/s10495-022-01712-5

Cited by 9 publications

(2 citation statements)

References 49 publications

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“…Through qPCR, ELISA, collagen staining, and other methods, miR-136-5P has been observed to be downregulated in the myocardial tissue in CME and LPS mice, whereas TNF, IL-6, and TnI are upregulated. Overexpression of miR-136-5P decreases myocardial cell inflammation and pyroptosis [13]. Immunofluorescence reporter gene detection analysis has confirmed that miR-136-5p inhibits the ATXN1L/Capicua axis, thereby upregulating pyrin domain containing 1 (PYDC1) by targeting ATXN1L, and competitively inhibits the binding of NLRP3 to ASC, thereby inhibiting inflammation and pyroptosis, and decreasing CME-induced cardiac injury [13].…”

Section: Roles Of Mirnas In the Inflammatory Response After Cmementioning

confidence: 98%

“…Overexpression of miR-136-5P decreases myocardial cell inflammation and pyroptosis [13]. Immunofluorescence reporter gene detection analysis has confirmed that miR-136-5p inhibits the ATXN1L/Capicua axis, thereby upregulating pyrin domain containing 1 (PYDC1) by targeting ATXN1L, and competitively inhibits the binding of NLRP3 to ASC, thereby inhibiting inflammation and pyroptosis, and decreasing CME-induced cardiac injury [13]. Chen et al have found that miR-200a-3p decreases after CME; consequently, myocardial injury induced by CME is ameliorated through inhibition of the TXNIP/ NLRP3 axis, the inflammatory response, and oxidative stress [19].…”

Section: Roles Of Mirnas In the Inflammatory Response After Cmementioning

confidence: 99%

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Advances in MicroRNA-Mediated Regulation of Cardiomyocyte Injury After Coronary Microembolization

Li,

Zheng,

et al. 2024

CVIA

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Coronary microembolization (CME) occurs in patients with acute coronary syndrome and is caused primarily by atherosclerotic plaque rupture associated with surgery. CME can lead to arrhythmias, decreased coronary blood flow reserve, and cardiac systolic dysfunction. The clinical efficacy of conventional coronary artery dilation, antiplatelet agents, and direct thrombus aspiration after CME is not satisfactory. Studies have indicated that microRNAs (miRNAs) specifically bind the 3′ untranslated regions (UTRs) of inflammatory response-, apoptosis-, and autophagy-related mRNAs, and ultimately affect CME prognosis. In-depth studies of the roles of miRNAs in CME occurrence and development would not only advance understanding of the mechanisms underlying poor prognosis after CME but also aid in identifying new targets for drug treatment. Here, we review the regulatory effects of miRNAs on myocardial cell injury after CME in terms of the inflammatory response, apoptosis, and autophagy. Overall, changes in miRNA levels after CME decrease myocardial autophagy and worsen cardiac prognosis. Current evidence suggests a potential strategic pathway for therapeutic intervention in CME management.

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Section: Roles Of Mirnas In the Inflammatory Response After Cmementioning

confidence: 98%

Section: Roles Of Mirnas In the Inflammatory Response After Cmementioning

confidence: 99%

Advances in MicroRNA-Mediated Regulation of Cardiomyocyte Injury After Coronary Microembolization

Li,

Zheng,

et al. 2024

CVIA

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miR‐136‐5p/FZD4 axis is critical for Wnt signaling‐mediated myogenesis and skeletal muscle regeneration

Zhang

Yin

Lin

et al. 2023

Journal Cellular Physiology

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Skeletal muscle can undergo a regenerative process in response to injury or disease to maintain muscle quality and function. Myogenesis depends on the proliferation and differentiation of myoblasts, and miRNAs can maintain the balance between them by precisely regulating many key factors in the myogenic network. Here, we found that miR‐136‐5p was significantly upregulated during the proliferation and differentiation of C2C12 cells. We demonstrate that miR‐136‐5p acts as a myogenic negative regulator during the development of mouse C2C12 myoblasts. In terms of mechanism, miR‐136‐5p inhibits the formation of β‐catenin/LEF/TCF DNA‐binding factor transcriptional regulatory complex by targeting FZD4, a gating protein in the Wnt signaling pathway, thereby enhancing downstream myogenic factors and finally promoting myoblast proliferation and differentiation. In addition, in BaCl2‐induced muscle injury mouse model, miR‐136‐5p knockdown accelerated the regeneration of skeletal muscle after injury, and further led to the improvement of gastrocnemius muscle mass and muscle fiber diameter, while being suppressed by shFZD4 lentivirus infection. In summary, these results demonstrate the essential role of miR‐136‐5p/FZD4 axis in skeletal muscle regeneration. Given the conservation of miR‐136‐5p among species, miR‐136‐5p may be a new target for treating human skeletal muscle injury and improving the production of animal meat products.

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Functional implications of paralog genes in polyglutamine spinocerebellar ataxias

Felício,

du Mérac,

Amorim

et al. 2023

Hum. Genet.

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Polyglutamine (polyQ) spinocerebellar ataxias (SCAs) comprise a group of autosomal dominant neurodegenerative disorders caused by (CAG/CAA)n expansions. The elongated stretches of adjacent glutamines alter the conformation of the native proteins inducing neurotoxicity, and subsequent motor and neurological symptoms. Although the etiology and neuropathology of most polyQ SCAs have been extensively studied, only a limited selection of therapies is available. Previous studies on SCA1 demonstrated that ATXN1L, a human duplicated gene of the disease-associated ATXN1, alleviated neuropathology in mice models. Other SCA-associated genes have paralogs (i.e., copies at different chromosomal locations derived from duplication of the parental gene), but their functional relevance and potential role in disease pathogenesis remain unexplored. Here, we review the protein homology, expression pattern, and molecular functions of paralogs in seven polyQ dominant ataxias—SCA1, SCA2, MJD/SCA3, SCA6, SCA7, SCA17, and DRPLA. Besides ATXN1L, we highlight ATXN2L, ATXN3L, CACNA1B, ATXN7L1, ATXN7L2, TBPL2, and RERE as promising functional candidates to play a role in the neuropathology of the respective SCA, along with the parental gene. Although most of these duplicates lack the (CAG/CAA)n region, if functionally redundant, they may compensate for a partial loss-of-function or dysfunction of the wild-type genes in SCAs. We aim to draw attention to the hypothesis that paralogs of disease-associated genes may underlie the complex neuropathology of dominant ataxias and potentiate new therapeutic strategies.

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MicroRNA-136-5p protects cardiomyocytes from coronary microembolization through the inhibition of pyroptosis

Cited by 9 publications

References 49 publications

Advances in MicroRNA-Mediated Regulation of Cardiomyocyte Injury After Coronary Microembolization

Advances in MicroRNA-Mediated Regulation of Cardiomyocyte Injury After Coronary Microembolization

miR‐136‐5p/FZD4 axis is critical for Wnt signaling‐mediated myogenesis and skeletal muscle regeneration

Functional implications of paralog genes in polyglutamine spinocerebellar ataxias

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