Publications by authors named "Shizhong Zheng"

Liver cancer treatment encounters considerable therapeutic challenges, especially because hypoxic microenvironments markedly reduce sensitivity to chemotherapeutic agents. TFAM (mitochondrial transcription factor A) plays a crucial role in maintaining mitochondrial function. Oroxylin A (OA), a flavonoid with potential therapeutic properties, demonstrated prospects in cancer treatment.

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Background: Heat stress is one of the main environmental factors limiting the growth, yield and quality of tea plants (). Trehalose involved in plant responses to multiple adverse environmental stresses, including heat stress. However, the roles of circular RNAs (circRNAs) and their involvement in the trehalose response to heat stress remain unknown.

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Objective: Cranioplasty is a common neurosurgical procedure aimed at providing structural protection to cerebral tissues and enhancing neurological function. The choice of implant material, particularly polyetheretherketone (PEEK) and titanium mesh, significantly influences postoperative outcomes, including the incidence of subgaleal fluid collections (SFC). This study investigates the incidence of SFC associated with PEEK and titanium mesh in cranioplasty, identifying risk factors and implications for clinical practice.

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Tendinopathy is one of the most prevalent sports injury diseases in orthopedics. However, there is no effective treatment or medicine. Recently, the discovery of tendon stem cells (TSCs) provides a new perspective to find new therapeutic methods for Tendinopathy.

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Type 1 insulin-like growth factor receptor (IGF1R) plays an important role in cancer, however, posttranscriptional regulation such as N-methyladenosine (mA) of IGF1R remains unclear. Here, we reveal a role for a lncRNA Downregulated RNA in Cancer (DRAIC) suppress tumor growth and metastasis in clear cell Renal Carcinoma (ccRCC). Mechanistically, DRAIC physically interacts with heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1) and enhances its protein stability by blocking E3 ligase F-box protein 11 (FBXO11)-mediated ubiquitination and proteasome-dependent degradation.

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It is well known that application of exogenous trehalose can enhance the heat resistance of plants. To investigate the underlying molecular mechanisms by which exogenous trehalose induces heat resistance in , a combination of physiological and transcriptome analyses was conducted. The findings revealed a significant increase in the activity of superoxide dismutase (SOD) and peroxidase (POD) upon treatment with 5.

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Background: Traditional Chinese medicine (SB), one of the clinical firstline heat-clearing drugs, has obvious symptomatic advantages for hepatic fibrosis with dampness-heat stasis as its syndrome. We aim to predict and validate the potential mechanism of active ingredients against liver fibrosis more scientifically and effectively.

Methods: The underlying mechanism of in inhibiting hepatic fibrosis was studied by applying network pharmacology, molecular docking and molecular dynamics simulation.

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Background And Aims: Development of fibrosis in chronic liver disease requires activation of hepatic stellate cells (HSCs) and leads to a poor outcome. Artesunate (Art) is an ester derivative of artemisinin that can induce ferroptosis in HSCs, and activated transcriptional factor 3 (ATF3) is an ATF/CREB transcription factor that is induced in response to stress. In this study, we examined the role of the Rho-associated protein kinase 1 (ROCK1)/ATF3 axis in Art-induced ferroptosis in HSCs.

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Hepatocellular carcinoma (HCC) is one of the most common malignancy, presenting a formidable challenge to the medical community owing to its intricate pathogenic mechanisms. Although current prevention, surveillance, early detection, diagnosis, and treatment have achieved some success in preventing HCC and controlling overall disease mortality, the imperative to explore novel treatment modalities for HCC remains increasingly urgent. Epigenetic modification has emerged as pivotal factors in the etiology of cancer.

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Background & Aims: Although ferroptosis holds promise as a new strategy for treating hepatocellular carcinoma (HCC), there are several obstacles that need to be overcome. One major challenge is the lack of understanding about the mechanisms underlying ferroptosis. Additionally, while the mA modification has been shown to regulate various forms of cell death, its role in regulating ferroptosis in HCC has been largely overlooked.

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COVID-19 is mainly characterized by respiratory disorders and progresses to multiple organ involvement in severe cases. With expansion of COVID-19 and SARS-CoV-2 research, correlative liver injury has been revealed. It is speculated that COVID-19 patients exhibited abnormal liver function, as previously observed in the SARS and MERS pandemics.

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Background And Aims: Aerobic glycolysis reprogramming occurs during HSC activation, but how it is initiated and sustained remains unknown. We investigated the mechanisms by which canonical Wnt signaling regulated HSC glycolysis and the therapeutic implication for liver fibrosis.

Approach And Results: Glycolysis was examined in HSC-LX2 cells upon manipulation of Wnt/β-catenin signaling.

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Formed by L-phenylalanine (L-phe) ammonia under the action of aromatic amino acid aminotransferases (AAATs), volatile benzenoids (VBs) and volatile phenylpropanoids (VPs) are essential aromatic components in oolong tea (). However, the key VB/VP components responsible for the aromatic quality of oolong tea need to be revealed, and the formation mechanism of VBs/VPs based on AAAT branches during the post-harvest process of oolong tea remains unclear. Therefore, in this study, raw oolong tea and manufacturing samples were used as the test materials, and targeted metabolomics combined with transcriptome analysis was also conducted.

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Background And Purpose: Senescence in hepatic stellate cells (HSCs) limits liver fibrosis. Glutaminolysis promotes HSC activation. Here, we investigated how emodin affected HSC senescence involving glutaminolysis.

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In recent study, the pathological mechanism of liver fibrosis has been associated with hepatic stellate cell (HSC) senescence. Targeted induction of HSC senescence is considered as a new strategy to remove activated HSC. Nevertheless, little is known about the role of ferritinophagy in cell senescence.

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Background: LSECs (Liver sinusoidal endothelial cells) are the portal of liver, their pathological angiogenesis plays a constructive role in etiopathogenesis of liver fibrosis by affecting liver tissue repair and inflammatory drive. Although intervention in angiogenesis can effectively inhibit abnormal activation of LSEC, no effective drugs have been found to treat liver fibrosis.

Purpose: We investigated the effect of the natural compound Curcumol on LSEC angiogenesis and elucidated the novel underlying mechanism, expecting to provide a scientific basis for exploring potential therapeutic drugs for liver fibrosis.

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Liver fibrosis is an early pathological feature of hepatic diseases. Hepatic stellate cell (HSC) activation and disordered proliferation are associated with liver fibrosis. The present study identified significant differences in the expression levels of microRNA (miRNA/miR)‑29b‑3p in clinical samples and multiple miRNA databases.

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Background: The most significant cause of treatment failure in chronic myeloid leukemia (CML) is a persistent population of minimal residual cells. Emerging evidences showed that methylation of SHP-1 contributed to Imatinib (IM) resistance. Baicalein was reported to have an effect on reversal of chemotherapeutic agents resistance.

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The roles of nuclear receptor subfamily 1 group d member 1 (NR1D1) and the circadian clock in liver fibrosis remain unclear. Here, we showed that liver clock genes, especially NR1D1, were dysregulated in mice with carbon tetrachloride (CCl)-induced liver fibrosis. In turn, disruption of the circadian clock exacerbated experimental liver fibrosis.

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Relevant studies have recognized the important role of hepatic stellate cell (HSC) senescence in anti-liver fibrosis. Cellular senescence is believed to be regulated by the cGAS-STING signaling pathway. However, underlying exact mechanisms of cGAS-STING pathway in hepatic stellate cell senescence are still unclear.

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Background And Aims: Naringenin is an anti-inflammatory flavonoid that has been studied in chronic liver disease. The mechanism specific to its antifibrosis activity needs further investigation This study was to focused on the cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS) pathway in hepatic stellate cells and clarified the antifibrosis mechanism of naringenin.

Methods: The relationship between the cGAS-stimulator of interferon genes (STING) pathway and liver fibrosis was analyzed using the Gene Expression Omnibus database.

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Background And Aims: Recognition of excessive activation of hepatic stellate cells (HSCs) in liver fibrosis prompted us to investigate the regulatory mechanisms of HSCs. We aimed to examine the role of O-GlcNAcylation modification of alanine, serine, cysteine transporter 2 (ASCT2) in HSCs and liver fibrosis.

Methods: The expression of O-GlcNAcylation modification in fibrotic mice livers and activated HSCs was analyzed by western blotting.

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Background: Qingchang Wenzhong Decoction (QCWZD), a chinese herbal prescription, is widely used for ulcerative colitis (UC). Nevertheless, the active ingredients and mechanism of QCWZD in UC have not yet been explained clearly.

Purpose: This research focuses on the identification of the effective ingredients of QCWZD and the prediction and verification of their potential targets.

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Senescence of activated hepatic stellate cells (aHSCs) is a stable growth arrest that is implicated in liver fibrosis regression. Senescent cells often accompanied by a multi-faceted senescence-associated secretory phenotype (SASP). But little is known about how alanine-serine-cysteine transporter type-2 (ASCT2), a high affinity glutamine transporter, affects HSC senescence and SASP during liver fibrosis.

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