Xiuyi Huang

The First Affiliated Hospital, Sun Yat-sen University

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Yunchong Liu

Sun Yat-sen University

Zilun Li

The First Affiliated Hospital, Sun Yat-sen University

Kan Huang

The First Affiliated Hospital, Sun Yat-sen University

Zhengde Zhao

Sun Yat-sen University

Zhipeng Cen

Sun Yat-sen Memorial Hospital

Tengyao Wang

Sun Yat-sen Memorial Hospital

Renli Zeng

Sun Yat-sen Memorial Hospital

Sifan Chen

Sun Yat-sen University

Chenshu Liu

University of California, Berkeley

Dongxiao Fan

The First Affiliated Hospital, Sun Yat-sen University

Cooperative Institutions

Sun Yat-sen University

Sun Yat-sen Memorial Hospital

The First Affiliated Hospital, Sun Yat-sen University

Guangzhou Medical University

Sichuan University

Guangzhou Eighth People's Hospital

West China Hospital of Sichuan University

Chinese Academy of Sciences

University of Chinese Academy of Sciences

Gulf University

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Distance metric-based forest cover change detection using MODIS time series

AGU Fall Meeting Abstracts (2012)

Xiuyi Huang M. A. Friedl Damien Sulla‐Menashe

Forest cover

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Hypoxia-inducible factor-1α inhibitor promotes non-alcoholic steatohepatitis development and increases hepatocellular lipid accumulation via TSKU upregulation

Archives of Biochemistry and Biophysics (2025)

Renli Zeng Yuxin Wang Jielu Wen Zhipeng Cen Tengyao Wang

Steatohepatitis

Hypoxia

Hypoxia-Inducible Factors

10.1016/j.abb.2025.110313

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The Profile of Secondary Glaucoma in China: A Study of Over 10,000 Patients

Journal of Glaucoma (2021)

Haijun Gong Jiawei Ren Bingru Zheng Xiuyi Huang Yunru Liao

Few studies have investigated the epidemiology of secondary glaucoma (SG) in China. This study analyzed the current profile of admitted patients with SG at the largest ophthalmic center in China.SG cases were retrieved retrospectively by International Classification of Disease-10 clinical coding data from January 2010 to December 2019. Demographic data, etiologies, and the management of SG were analyzed. The ratios of the etiologies were compared with previously reported data from other regions. The etiologies and management between the 2010 to 2014 group and the 2015 to 2019 group were compared.A total of 11,730 cases were enrolled. The mean age of the patients with SG was 44.45±19.45 years old. Men (66.94%) were more vulnerable than women (33.06%). The etiologies of SG in 2010 to 2019 were trauma (28%), vascular disease (18%), lens-induced (9%), inflammation (11%), drug-induced (2%), anterior segment surgery (7%), posterior segment surgery (11%), syndrome-associated (4%), and tumors (1%). Compared with other regions, our data have a higher proportion of trauma and vascular disease-associated SG. Compared with 2010 to 2014, trauma-induced SG declined, and drug-induced SG, anterior segment surgery, and syndrome-associated SG increased in 2015 to 2019 (P<0.001). Vascular disease-associated SG cases were older than trauma-induced SCs and had a higher percentage in retired patients (P<0.001), whereas trauma-induced SGs were more prevalent in pediatric patients than vascular disease-related SGs (P<0.001). In addition, the application of drainage device implantation, cataract surgery, and cyclophotocoagulation increased, whereas trabeculectomy and anterior chamber paracentesis and cyclocryotherapy decreased in 2015 to 2019 (P<0.005).Although the etiology spectrum has changed during the last 10 years, trauma and vascular disease are still common causes of SG in southern China. Traditional antiglaucoma surgery decreased gradually, and more advanced treatments emerged for its treatment. Up-to-date knowledge of SGs reflects the impact of economic development and ophthalmic service improvement on SGs and is of great value for ophthalmologists to detect SGs early and manage them in a timely manner.

Etiology

10.1097/ijg.0000000000001924

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Celastrol directly binds with VAMP7 and RAB7 to inhibit autophagy and induce apoptosis in preadipocytes

Frontiers in Pharmacology (2023)

Chenshu Liu Na Li Meixiu Peng Kan Huang Dongxiao Fan

Obesity is one of the most prevalent chronic metabolic diseases, and induction of apoptosis in preadipocytes and adipocytes is a potential strategy to treat obesity. Celastrol represents one of the most robust anti-obesity phytochemicals so far, yet its direct binding target remains elusive. Here, we determined that celastrol could induce apoptosis in preadipocytes via mitochondrial mediated pathway. Further study clarified that celastrol inhibited the fusion of autophagosome and lysosome to prohibit autophagy, leading to cell apoptosis. By conducting virtual screening and genetic manipulation, we verified that overexpression of VAMP7 and RAB7 could block the effects of celastrol on inhibiting autophagy and inducing apoptosis. The Surface Plasmon Resonance study confirmed the direct binding of celastrol with VAMP7 and RAB7. The functional study illustrated the inhibition of RAB7 GTPase activity after celastrol treatment. Moreover, celastrol induced comparable apoptosis in murine epididymal adipose tissue, human preadipocytes and adipocytes, but not in human hepatocytes. An inhibitory effect on differentiation of human primary visceral preadipocytes was also observed. In conclusion, celastrol exhibited inhibitory effect of autophagy via direct binding with VAMP7 and RAB7, leading to an increase in preadipocytes apoptosis. These results advance our understanding in the potential application of celastrol in treating obesity.

Celastrol

Autophagosome

10.3389/fphar.2023.1094584

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Time-restricted feeding ameliorates non-alcoholic fatty liver disease through modulating hepatic nicotinamide metabolism via gut microbiota remodeling

Gut Microbes (2024)

Ruijia Feng Wenchao Yang Weiqi Feng Xiuyi Huang Meifeng Cen

Non-alcoholic fatty liver disease (NAFLD) has emerged as a global health concern, lacking specific therapeutic strategies. Time-restricted feeding (TRF) regimen demonstrated beneficial effects in NAFLD; however, the underlying mechanisms remain unclear. In this study, we established a NAFLD mouse model through a high-fat diet (HFD) and implemented the 16:8 TRF regimen for a duration of 6 weeks. We demonstrated that TRF remarkably alleviated hepatic steatosis in HFD mice. Of note, aldehyde oxidase 1 (AOX1), a key enzyme in hepatic nicotinamide (NAM) catabolism, exhibited apparent upregulation in response to HFD, leading to abnormal accumulation of N-Methyl-6-pyridone-3-carboxamide (N-Me-6-PY, also known as 2PY) and N-Methyl-4-pyridone-5-carboxamide (N-Me-4-PY, also known as 4PY), whereas it was almost restored by TRF. Both N-Me-6-PY and N-Me-4-PY promoted de novo lipogenesis and fatty acid uptake capacities in hepatocyte, and aggravated hepatic steatosis in mice either fed chow diet or HFD. In contrast, pharmacological inhibition of AOX1 was sufficient to ameliorate the hepatic steatosis and lipid metabolic dysregulation induced by HFD. Moreover, transplantation of fecal microbiota efficiently mimicked the modulatory effect of TRF on NAM metabolism, thus mitigating hepatic steatosis and lipid metabolic disturbance, suggesting a gut microbiota-dependent manner. In conclusion, our study reveals the intricate relationship between host NAM metabolic modification and gut microbiota remodeling during the amelioration of NAFLD by TRF, providing promising insights into the prevention and treatment of NAFLD.

Fatty Acid Metabolism

10.1080/19490976.2024.2390164

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Tumor-Targeting Multifunctional Nanoprobe for Enhanced Photothermal/Photodynamic Therapy of Liver Cancer

Langmuir (2021)

Bei Li Xiaoya Niu Maodi Xie Fan Luo Xiuyi Huang

Numerous researchers have committed to the development of combined therapy strategies for tumors, since their use in the treatment of tumors has more ideal therapeutic outcomes. In the study, we designed and prepared gold nanostars with CD147 modified on the surface and then efficiently loaded a photosensitive drug IR820 to construct a multifunctional nanoprobe. Due to the protection effect of gold, the nanoprobe has oxygen/heat energy generation capability and can also efficiently deliver the loaded drugs inside the tumor cells. Moreover, the nanoprobe has excellent photothermal/photodynamic therapeutic outcomes. The observation by photoacoustic real-time imaging validated the outstanding tumor-targeting characteristics of our nanoprobe. Finally, in the in vivo treatment experiment, the nanoprobe achieved ideal tumor-suppressive effects after the photothermal/photodynamic therapy. In summary, the findings of this experiment are useful in the development of new combined tumor therapy strategies based on nanomaterials.

Nanoprobe

Cancer Treatment

Nanomaterials

10.1021/acs.langmuir.0c03578

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Mesenchymal Stem/Stromal Cells Therapy for Metabolic Syndrome: Potential Clinical Application?

Stem Cells (2023)

Xiuyi Huang Yunchong Liu Zilun Li Lilach O. Lerman

Abstract Mesenchymal stem/stromal cells (MSCs), a class of cells with proliferative, immunomodulatory, and reparative functions, have shown therapeutic potential in a variety of systemic diseases, including metabolic syndrome (MetS). The cluster of morbidities that constitute MetS might be particularly amenable for the application of MSCs, which employ an arsenal of reparative actions to target multiple pathogenic pathways simultaneously. Preclinical studies have shown that MSCs can reverse pathological changes in MetS mainly by inhibiting inflammation, improving insulin resistance, regulating glycolipid metabolism, and protecting organ function. However, several challenges remain to overcome before MSCs can be applied for treating MetS. For example, the merits of autologous versus allogeneic MSCs sources remain unclear, particularly with autologous MSCs obtained from the noxious MetS milieu. The distinct characteristics and relative efficacy of MSCs harvested from different tissue sources also require clarification. Moreover, to improve the therapeutic efficacy of MSCs, investigators have explored several approaches that improved therapeutic efficacy but may involve potential safety concerns. This review summarized the potentially useful MSCs strategy for treating MetS, as well as some hurdles that remain to be overcome. In particular, larger-scale studies are needed to determine the therapeutic efficacy and safety of MSCs for clinical application.

Cell therapy

Regenerative Medicine

10.1093/stmcls/sxad052

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Gut microbial co-metabolite 2-methylbutyrylcarnitine exacerbates thrombosis via binding to and activating integrin α2β1

Cell Metabolism (2024)

Kan Huang Zilun Li Xi He Jun Dai Bingding Huang

10.1016/j.cmet.2024.01.014

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Screening plasma metabolites as potential biomarkers for type B aortic dissection

Cardiovascular Diagnosis and Therapy (2023)

Heng Xu Dongxiao Fan Yupeng Lin Chenshu Liu Kan Huang

Background: Aortic dissection (AD) is a serious aortic disease. Although current imaging methods can provide accurate diagnosis for AD, they do not include essential biological information. The aim of this study is to identify plasma metabolites for the risk and severity of type B AD (TBAD). Methods: In this cross-sectional study, we enrolled 16 hypertensive patients with TBAD and 7 hypertensive patients without TBAD in Jieyang People’s Hospital between December 2021 and April 2022. After plasma metabolomics analysis, a metabolites risk score (MRS) model was conducted through logistic regression and least absolute shrinkage and selection operator (LASSO) regression to predict the risk of TBAD. Subsequently, TBAD group was divided into uncomplicated and complicated TBAD subgroups for further screening for metabolites related to the severity of TBAD. Results: Three metabolites, including 1,5-anhydro-D-glucitol, D-(+)-sucrose and PC(O-16:0/0:0) were related to the risk of TBAD. Compared to hypertensive patients without TBAD, the abundance of 1,5-anhydro-D-glucitol and D-(+)-sucrose were significantly increased while PC(O-16:0/0:0) was significantly reduced in hypertensive patients with TBAD (P<0.001). We subsequently built an MRS model based on these three metabolites. Furthermore, we found that hydrocinnamic acid (r=0.741, P<0.001) was independently correlated with the TBAD severity, while glycine deoxycholic acid (r=−0.538, P=0.008) and glycochenodeoxycholic acid (r=−0.538, P=0.008) were inversely correlated with the TBAD severity independently. Conclusions: The present study screened out three plasma metabolites associated with the risk of TBAD, constructed an MRS model, and identified three metabolites that were independently associated with the severity of TBAD. These findings may serve to identify more TBAD-related biomarkers and shed light on exploring potential mechanisms of TBAD.

10.21037/cdt-23-183

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The effects and mechanism of hypoxia-inducible factor-1α inhibitor, a potential therapy strategy, on non-alcoholic steatohepatitis

Authorea (Authorea) (2023)

Renli Zeng Jielu Wen Zhipeng Cen Tengyao Wang Meng Duan

Non-alcoholic steatohepatitis (NASH) is the progressive form of non-alcoholic fatty liver disease (NAFLD) which is the most common chronic liver disease worldwide. However, there are no FDA-approved drugs for treating NASH. The roles of hypoxia-inducible factor-1α (HIF1α) playing in NASH are not fully understood, and the mainstream view is that HIF1α knockout improved NASH. Here, in order to explore the clinical translation potential of HIF1α, we used HIF1α inhibitor KC7F2 to treat diet-induced NASH mice for 10 weeks. Surprisingly, it turned out that KC7F2 intensified liver lipid accumulation, inflammation, and fibrosis in NASH mice. Mechanistically, a most remarkable increase of expression of hepatokine Tsukushi (TSKU) was observed among twenty metabolism-related hepatokines in the liver of NASH mice after KC7F2 treatment. In vitro, we confirmed that inhibiting HIF1α or TSKU overexpression both significantly intensified lipid accumulation in hepatocytes, but didn’t increase expression of inflammation markers in LPS-induced macrophages or fibrosis markers in TGFβ-induced hepatic stellate cells. Moreover, Tsku knockdown reversed the HIF1α inhibitor-induced lipid accumulation in hepatocytes. Taken together, we first found that HIF1α inhibitor exacerbated NASH presumably via promoting hepatocyte lipid accumulation which was dependent on TSKU, indicating NASH may be a contraindication for HIF1α inhibitor rather than an indication.

Steatohepatitis

Hepatic stellate cell

10.22541/au.169990088.86311683/v1

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