Mitochondria are an important target of photobiomodulation in cardiomyocytes

Photobiomodulation(PBM)has been shown to delay the pathological process of heart failure,but the exact mechanism of action is not clear.Mitochondria occupy one-third of the volume of mammalian cardiomyocytes(CMs)and are central transport stations for CM energy metabolism.Therefore,in this study,we explored the regulatory effects of 630 nm light-emitting diodes(LED-Red)on the mitochondria of CMs.The results show that LED-Red-based PBM promotes adenosine triphosphate(ATP)synthesis by upregulating the expression of glycolipid metabolizing enzymes.Correspondingly,there was an improvement in the activity of succinate dehydrogenase(SDH),a key enzyme in the mitochondrial electron transport chain,and the mitochondrial membrane potential.Meanwhile,LED-Red affected the state of mitochondrial oxidative stress and promoted the generation of reactive oxygen species(ROS),but the increased ROS production did not damage the CMs.In addition,mitochondrial division and fusion were also affected by the stimulation of LED-Red.Finally,PBM treatment led to a significant increase in transcript levels of mitochondrial transcription factor A(TFAM),which controls the stability of the mitochondrial genome.Collectively,irradiation with LEDs at 630 nm played a regulatory role in mitochondrial function,suggesting that mitochondria appear to be the recipients of PBM treatment.This study provides more insights into the mechanisms underlying PBM treatment in heart diseases.

LncRNA ZFAS1 regulates cardiomyocyte differentiation of human embryonic stem cells

Background:Cardiomyocytes derived from human embryonic stem cells(hESCs)are regulated by complex and stringent gene networks during differentiation.Long non-coding RNAs(lncRNAs)exert critical epigenetic regulatory functions in multiple differentiation processes.However,the involvement of lncRNAs in the differentiation of hESCs into cardiomyocytes has not yet been fully elucidated.Here,we identified the key roles of ZFAS1(lncRNA zinc finger antisense 1)in the differentiation of cardiomyocytes from hESCs.Methods:A model of cardiomyocyte differentiation from stem cells was established using the monolayer differentiation method,and the number of beating hESCs-derived cardiomyocytes was calculated.Gene expression was analyzed by quantitative real-time PCR(qRTPCR).Immunofluorescence assays were performed to assess the expression of cardiac troponin T(cTnT)andα-actinin protein in cardiomyocytes.Results:qRT-PCR showed that ZFAS1 expression in the mesoderm was significantly higher than that in embryonic stem cells,cardiac progenitor cells,and cardiomyocytes.Knockdown of ZFAS1 inhibited cardiomyocyte differentiation from hESCs,which was characterized by reduced expression of the cardiac-specific markers cTnT,α-actinin,myosin heavy chain 6(MYH6),and myosin heavy chain 7(MYH7).In contrast,ZFAS1 overexpression remarkably increased the percentage of spontaneously beating cardiomyocytes.In terms of the mechanism,we found that ZFAS1 is an antisense lncRNA at the 5′end of the protein-coding gene ZNFX1.Knockdown of ZFAS1 could increase the mRNA expression level of ZNFX1.Furthermore,qRT-PCR demonstrated that the silencing of ZNFX1 led to an increase in cardiac-specific markers that predicted the promotion of cardiomyocyte differentiation.Conclusion:Altogether,these data suggest that lncRNA-ZFAS1 is required for cardiac differentiation by functionally inhibiting the expression of ZNFX1,which may provide a reference for the treatment of heart disease to a certain extent.

The multiple mechanisms of tripterygium wilfordii-induced acute kidney injury based on network pharmacology and molecular docking

Acute kidney injury(AKI)is a common and serious health issue with a growing incidence and mortality rate.Tripterygium wilfordii(TW)is a traditional Chinese medicine that has been reported to cause kidney damage.However,the associated mechanism of TW-induced AKI remains unclear.Therefore,we aimed to uncover the associated mechanisms of AKI induced by TW using network pharmacology and bioinformatics.The candidate compounds of TW and the potential targets were screened using TCMSP and CTD database,and the AKI-related targets were identified from the Dis Ge NET database.The disease targets were intersected with the drug targets,and the Wayne diagram was drawn by Venny 2.1.0 software.We developed proteinprotein interactions(PPI)network and the“disease-compound-target-pathway”network through the Cytoscape software.By using the DAVID database,GO and KEGG enrichment analysis was carried out to reveal the potential signaling pathways of the compound-TW-induced AKI.Meanwhile,the Auto dock vina 1.1.2 was used for molecular docking to verify the active compound and key targets’binding ability.Critical compounds and key targets of TW-induced AKI were identified,including triptolide,kaempferol,β-sitosterol,nobiletin,stigmasterol,TNF,and so on.The GO analysis showed that potential genes’biological function was mainly involved in apoptosis,oxidative stress,and inflammation.Moreover,eight signaling pathways were found,including the HIF-1 signaling pathway,VEGF signaling pathway,apoptosis,and so on.The molecular docking results proved that the core compound’s affinity with the corresponding protein of the gene targets was good.This study preliminarily predicted the core toxic compounds,targets,and related pathways of TW-induced AKI,providing a theoretical basis for the follow-up clinical rational drug use and related research work of TW.

Cyclin L1 controls cardiomyocyte proliferation and heart repair after injury

Dear Editor,Myocardial infarction(MI)is characterized by the loss of functional cardiomyocyte(CM)in the heart,resulting in cardiac systolic dysfunction and heart failure.1,2 Increasing evidence suggested that in the heart of neonatal mice after apical resection(AR),the CM can proliferate and regenerate myocardium to repair the heart.While in the heart of adult mice after MI,the CM loses the ability to re-enter the cell cycle but undergoes hypertrophic growth.

A compact complex-coefficient microwave photonic filter with continuous tunability

A complex-coefficient microwave photonic filter with continuous tunability is proposed and demonstrated,which has a compact structure and stable performance without splitting the optical path and tuning the polarization state. By only controlling the DC biases of the modulator, the amplitudes and the phases of the filter taps can both be tuned. The phase difference between the two filter taps covers a full 360° range from 10 GHz to 32 GHz. Frequency responses of the proposed filter are measured within 10–20 GHz with different center frequencies.