Publications by authors named "Xiyang Peng"

Background: Skeletal muscle atrophy is one of the main side effects of high-dose or continuous use of glucocorticoids (such as dexamethasone). However, there are limited studies on dexamethasone-induced skeletal muscle atrophy in zebrafish and even fewer explorations of the underlying molecular mechanisms. This study aimed to construct a model of dexamethasone-induced skeletal muscle atrophy in zebrafish and to investigate the molecular mechanisms.

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Sarcopenia is one of the most common skeletal muscle disorders and is characterized by infirmity and disability. While extensive research has focused on elucidating the mechanisms underlying the progression of sarcopenia, further comprehensive insights into its pathogenesis are necessary to identify new preventive and therapeutic approaches. The involvement of inflammasomes in sarcopenia is widely recognized, with particular emphasis on the NLRP3 (NLR family pyrin domain containing 3) inflammasome.

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Congenital heart defects (CHDs) are common human birth defects. Genetic mutations potentially cause the exhibition of various pathological phenotypes associated with CHDs, occurring alone or as part of certain syndromes. Zebrafish, a model organism with a strong molecular conservation similar to humans, is commonly used in studies on cardiovascular diseases owing to its advantageous features, such as a similarity to human electrophysiology, transparent embryos and larvae for observation, and suitability for forward and reverse genetics technology, to create various economical and easily controlled zebrafish CHD models.

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Sarcopenia is a common skeletal muscle degenerative disease characterized by decreased skeletal muscle mass and mitochondrial dysfunction that involves microRNAs (miR) as regulatory factors in various pathways. Exercise reduces age-related oxidative damage and chronic inflammation and increases autophagy, among others. Moreover, whether aerobic exercise can regulate mitochondrial homeostasis by modulating the miR-128/insulin-like growth factor-1 (IGF-1) signaling pathway and can improve sarcopenia requires further investigation.

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Article Synopsis
  • * In this study using zebrafish, researchers provided a high-fat diet to induce NAFLD and then included swimming exercise, which significantly improved liver health and reduced inflammation after 12 weeks.
  • * Results indicated that exercise enhanced mitochondrial structure and function, activated pathways promoting mitochondrial health, and partially restored mitophagy processes in the liver, suggesting swimming could be a beneficial treatment for NAFLD.
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The Popeye domain-containing protein 3 (POPDC3), a transmembrane protein with a unique cyclic adenosine monophosphate (cAMP) binding site, is widely expressed in mammalian tissues, with the highest levels of expression in skeletal muscle. POPDC3 plays a key role in many physiological and pathological processes and is considered a candidate biomarker and potential therapeutic target of cancer. In addition, POPDC3 gene variants have been associated with limb-girdle muscular dystrophy (LGMD) type 26.

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Introduction: Pericardial effusion is a common complication without a standard postoperative effusion treatment after cardiac surgery. The grooved negative pressure drainage tube has many advantages as the emerging alternative for drainage of pericardial effusion, such as it changes the structure of the traditional side hole, uses the capillary function to ensure drainage smooth, etc. The purpose of this study was to assess the feasibility and effectiveness of transthoracic color Doppler ultrasound-guided grooved negative pressure drainage tube implantation in pericardial effusion after cardiac surgery.

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Article Synopsis
  • Sarcopenia, a significant disorder in older adults, causes a gradual decline in muscle function, but exercise can help prevent or slow its development.
  • A study using 21-month-old zebrafish showed that they experience reduced swimming ability, muscle deterioration, and increased oxidative stress, making them a useful model for studying sarcopenia.
  • After eight weeks of exercise, the zebrafish displayed improvements, with changes in mitochondrial function linked to the activation of certain cellular pathways, suggesting new targets for treating age-related sarcopenia through exercise.
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Context: Bushen Yiyuan recipe (BYR) is an effective Chinese prescription with antifatigue and antioxidation effects.

Objective: The effects of BYR on testosterone synthesis in rat Leydig cells with exercise-induced low serum testosterone levels (EILST) are assessed.

Materials And Methods: Thirty-two Sprague-Dawley rats were chronically trained for 6 weeks to establish an EILST model.

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Excessive alcohol consumption can cause alcoholic myopathy, but the molecular mechanism is still unclear. In this study, zebrafish were exposed to 0.5% alcohol for eight weeks to investigate the effect of alcohol on skeletal muscle and its molecular mechanism.

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Obesity is a highly prevalent disease that can induce metabolic syndrome and is associated with a greater risk of muscular atrophy. Mitochondria play central roles in regulating the physiological metabolism of skeletal muscle; however, whether a decreased mitochondrial function is associated with impaired muscle function is unclear. In this study, we evaluated the effects of a high-fat diet on muscle mitochondrial function in a zebrafish model of sarcopenic obesity (SOB).

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Herein, we aimed to establish an aerobic exercise-induced physiological myocardial hypertrophy zebrafish (Danio rerio) model and to explore the underlying molecular mechanism. After 4 weeks of aerobic exercise, the AMR and U of the zebrafish increased and the hearts were enlarged, with thickened myocardium, an increased number of myofilament attachment points in the Z-line, and increased compaction of mitochondrial cristae. We also found that the mTOR signaling pathway, angiogenesis, mitochondrial fusion, and fission event, and mitochondrial autophagy were associated with the adaptive changes in the heart during training.

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Non-alcoholic fatty liver disease (NAFLD) is a common disease that causes serious liver damage. Exercise is recognized as a non-pharmacological tool to improve the pathology of NAFLD. However, the antioxidative effects and mechanisms by which exercise ameliorates NAFLD remain unclear.

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Article Synopsis
  • 15-hydroxyprostaglandin dehydrogenase (15-PGDH) is an enzyme that helps break down prostaglandins, essential signaling molecules, and is expressed in various tissues throughout mammals.
  • This enzyme is involved in critical processes that could aid in preventing organ damage, improving bone marrow recovery, and enhancing tissue regeneration, making it a potential target for new therapies.
  • Additionally, 15-PGDH shows tumor-suppressing effects in cancers and is linked to aging, suggesting its importance in both cancer treatment and managing age-related diseases.
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Article Synopsis
  • Long-term imbalance between fatigue and recovery can lead to muscle weakness and atrophy, with previous research showing excessive exercise affects heart health.
  • A zebrafish model was developed to study the effects of excessive exercise on skeletal muscle, revealing decreased muscle fiber size and critical swimming speed.
  • RNA-seq analysis identified key genes and pathways associated with skeletal muscle atrophy, suggesting important insights for creating safe exercise programs and for treating exercise-induced muscle issues.
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Wnt/β-catenin signaling plays a key role in pathological cardiac remodeling in adults. The identification of a tissue-specific Wnt/β-catenin interaction factor may provide a tissue-specific clinical targeting strategy. encodes the core interaction factor of Wnt/β-catenin.

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Exercise-induced cardiac remodeling has aroused public concern for some time, as sudden cardiac death is known to occur in athletes; however, little is known about the underlying mechanism of exercise-induced cardiac injury. In the present study, we established an excessive exercise-induced pathologic cardiac hypertrophy model in zebrafish with increased myocardial fibrosis, myofibril disassembly, mitochondrial degradation, upregulated expression of the pathological hypertrophy marker genes in the heart, contractile impairment, and cardiopulmonary function impairment. High-throughput RNA-seq analysis revealed that the differentially expressed genes were enriched in the regulation of autophagy, protein folding, and degradation, myofibril development, angiogenesis, metabolic reprogramming, and insulin and FoxO signaling pathways.

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Physical activity (PA) is widely recognized as one of the important elements of personal healthy life. To date, as the development of wearable sensing technologies, it is possible to utilize wearable devices and machine learning algorithms to efficiently and accurately monitor PA types, intensity and its associated human pattern for many health applications. But there is a trade-off between less-attachment of wearable devices and achievement of high accuracy in existing PA recognition studies.

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Background: Previously, we first identified the human tripartite motifcontaining protein 45 (TRIM45) acts as a novel transcriptional repressor in mitogenactivated protein kinase (MAPK) signaling pathway. After that, the inhibitory role of TRIM45 in the development of tumor was gradually unveiled. However, the function of TRIM45 in the tumorigenesis of lung cancer has not been characterized.

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Magnetoreception is essential for magnetic orientation in animal migration. The molecular basis for magnetoreception has recently been elucidated in fruitfly as complexes between the magnetic receptor magnetoreceptor (MagR) and its ligand cryptochrome (Cry). MagR and Cry are present in the animal kingdom.

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Background: CXXC-type zinc-finger protein CXXC5 has been reported to be associated with the development of cardiovascular disease. Recently, through signaling pathway screening we found that CXXC5 activated Tgfβ and myocardial differentiation signaling pathways simultaneously. Although the physiological and pathological function of CXXC5 in many organs has been well elucidated, its function in heart remains unclear.

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CXXC5 is a member of the CXXC-type zinc-finger domain containing protein family, which is suggested to function in gene transcription, cell adhesion and cytoskeleton organization. Previous studies have revealed that CXXC5 is expressed in skeletal muscle, but whether it regulates skeletal myogenesis is yet unknown. Here, we screened for the possible signaling pathways in which CXXC5 might participate using luciferase gene reporters.

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Using the promoter for cardiac myosin light chain 2 (cmlc2) gene, an expression vector pTol2-cmlc2-IRES- EGFP for making heart-specific expression of exogenous gene in transgenic zebrafish was generated previously. Here, we reported the construction of a transgenic zebrafish line which stably expresses EGFP using this vector, and the effects of EGFP on the heart development and cardiac function of this transgenic zebrafish line were preliminarily analyzed. The results showed that the green fluorescence signal of cmlc2:EGFP line under fluorescence microscopy specifically expressed in heart and faithfully recapitulated both the spatial and temporal expression patterns of endogenous cmlc2 gene revealed by in situ hybridization in the early developmental stages.

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