Zhilin Xu

Zhilin Xu


Research Focus & Metrics

Academic Career Length

5Years (2022-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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7 January 2026 in Mediators of Inflammation
Verified
Journal Article
Open access
ZHZenghui Hao
Zenghui Hao
JHJinbao Han
Jinbao Han
TYTing Yao
Ting Yao
ZZZheng Zhao
Zheng Zhao
WFWei Fan
Wei Fan
ZXZhilin Xu
Zhilin Xu
Neonatal necrotizing enterocolitis (NEC) is an intestinal disease that occurs in the neonatal period. The purpose of this study was to investigate the role of 5′‐aminolevulinate synthase 2 (ALAS2) in NEC‐induced intestinal injury. In a neonatal mouse, NEC model was induced by high‐osmolarity formula and hypoxia‐cold stress, and ALAS2 expression was significantly downregulated in ileal tissues ( p < 0.01), coinciding with elevated oxidative stress (increased Fe 2+ /malondialdehyde [MDA] and decreased superoxide dismutase [SOD]), inflammation (increased TNF‐α/interferon‐gamma [IFN‐γ]), and ferroptosis activation (increased acyl‐CoA synthetase long‐chain family member 4 [ACSL4] and decreased ferritin heavy chain 1 [FTH1] with mitochondrial shrinkage). In vitro, tumor necrosis factor‐alpha (TNF‐α)/IFN‐γ‐treated intestinal epithelial cell (IEC) exhibited progressive ALAS2 suppression and increased necrosis. Crucially, lentivirus‐mediated ALAS2 overexpression reversed these effects, reducing cell necrosis by 22% while suppressing ferroptosis markers (Fe 2+ accumulation, lipid reactive oxygen species [ROS], and mitochondrial depolarization) and oxidative damage (decreased MDA and restored glutathione [GSH]/catalase [CAT]/SOD). Untargeted metabolomics further revealed ALAS2‐mediated modulation of nutrient metabolism and redox pathways. Collectively, ALAS2 ameliorates NEC by blocking oxidative stress‐driven ferroptosis in IECs, proposing a novel therapeutic target.

11 July 2022 in BMC Pediatrics
Verified
Journal Article
Open access
PDF file
JHJinbao Han
Jinbao Han
ZHZenghui Hao
Zenghui Hao
LWLong Wang
Long Wang
TYTing Yao
Ting Yao
WFWei Fan
Wei Fan
ZXZhilin Xu
Zhilin Xu
This study explored the feasibility of mesoplasty with end-to-side anastomosis in the treatment of different apple-peel mesenteric defects with high jejunal atresia. A retrospective analysis was performed on 42 premature infants admitted to the hospital between 2014 and 2021. Prenatal ultrasound scans revealed bowel dilatation. The patients experienced vomiting after birth and produced white or no meconium. Plain radiography showed double or triple bubble signs and the patients underwent emergency laparotomy. High jejunal atresia with different apple-peel atresia appearance was discovered intraoperatively, involving mobilization of the ileocecal region. Patients received end-to-side anastomosis between the enlarged blind pouch and atretic bowel, as well as mesoplasty. A jejunal feeding tube was placed trans-nasally. Patients were discharged after achieving full enteral feeding. We also reviewed the literature on the subject. Three patients died and 39 survived. The discharged patients were followed up for 12 months, and none showed post-operative complications such as intestinal obstruction, malnutrition, or chronic diarrhea. All surviving patients reached the expected height and weight for children of the same age. For cases of high jejunal atresia with apple-peel intestinal atresia, mesoplasty may be a good option to avoid postoperative volvulus.

30 October 2024 in PeerJ
Verified
Journal Article
Open access
PDF file
TYTing Yao
Ting Yao
ZHZenghui Hao
Zenghui Hao
WFWei Fan
Wei Fan
JHJinbao Han
Jinbao Han
SWShuyu Wang
Shuyu Wang
ZXZhilin Xu
Zhilin Xu
Background: Hirschsprung’s disease (HSCR) is a congenital disorder characterized by aganglionosis in the intermuscular and submucosal nerve plexuses of the gut, leading to impaired gastrointestinal function. Although the precise cause and pathophysiology of HSCR remain elusive, increasing evidence points to a significant role of autophagy in its development, warranting further investigation into its underlying mechanisms. Methods: This study utilized publicly available microarray expression profiling datasets, GSE96854 and GSE98502, from the Gene Expression Omnibus (GEO). The R software (version 4.2.0) was employed to identify autophagy-related genes potentially showing differential expression in HSCR. Subsequent analyses included correlation analysis, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment, and protein-protein interaction (PPI) network analysis using the STRING database (version 11.0) and Cytoscape software (version 3.8.2). Ultimately, HSCR samples were used to verify the mRNA levels of important genes by quantitative real-time polymerase chain reaction (qRT-PCR) in a laboratory setting. Results: We have discovered 20 genes that are involved in autophagy and show variable expression. Among these genes, 15 are up-regulated and five are down-regulated. The enrichment analysis using the GO and KEGG pathways revealed a notable enrichment in pathways related to the control of autophagy. Nine hub genes were found via the investigation of the PPI network constructed from STRING database and module analysis using Cytoscape. Moreover, the concordance between SIRT1 expression in the HSCR model and the bioinformatics analysis of mRNA chip findings was validated using qRT-PCR. Conclusion: Utilizing bioinformatics analysis, we identified 20 potential genes associated with Hirschsprung’s disease that play a role in autophagy. Notably, the upregulation of SIRT1 may profoundly influence the progression of HSCR by regulating autophagy-related pathways, offering a novel perspective on the disease’s pathogenesis.

15 September 2023 in Research Square
Verified
Preprint
Open access
PDF file
TYTing Yao
Ting Yao
ZHZenghui Hao
Zenghui Hao
WFWei Fan
Wei Fan
JHJinbao Han
Jinbao Han
SWShuyu Wang
Shuyu Wang
ZXZhilin Xu
Zhilin Xu
Background Hirschsprung's disease (HSCR) is a congenital disorder characterized by aganglionosis in the intermuscular and submucosal nerve plexus of the intestines, resulting in impaired gastrointestinal function. The exact etiology and pathogenesis of HSCR are yet not fully understood. Accumulating evidence suggests that autophagy plays an important role in the pathogenesis of HSCR, but its specific mechanism needs to be further studied. Methods This study used the online Gene Expression Omnibus (GEO) microarray expression profiling datasets GSE96854 and GSE98502. R software was used to identify autophagy-related genes that displayed potential differential expression in HSCR. The differentially expressed autophagy-related genes were analyzed using correlation analysis, tissue-specific gene expression profiling, gene ontology (GO) enrichment analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, and protein-protein interaction (PPI) network analysis. Finally, HSCR specimens were utilized for in vitro verification of mRNA levels of key genes using quantitative real-time polymerase chain reaction (qRT-PCR). Results A total of 20 autophagy-related genes exhibiting differential expression were identified, comprising 15 up-regulated and five down-regulated genes. Enrichment analysis with the GO and KEGG pathways revealed significant enrichment in pathways associated with the regulation of autophagy, specifically macroautophagy. By conducting PPI network analysis and constructing key modules, we identified nine hub genes. Subsequently, the consistency between SIRT1 expression in the HSCR model and bioinformatics analysis of mRNA chip results was confirmed through qRT-PCR validation. Conclusion Through bioinformatics analysis, we identified 20 potential autophagy-related genes associated with HSCR. Among them, the upregulation of SIRT1 expression may impact the occurrence and progression of HSCR by regulating autophagy pathways. This provides a fresh outlook on the etiology of Hirschsprung's disease.

31 May 2022 in Research Square
Verified
Preprint
Open access
PDF file
JHJinbao Han
Jinbao Han
ZHZenghui Hao
Zenghui Hao
LWLong Wang
Long Wang
TYTing Yao
Ting Yao
WFWei Fan
Wei Fan
ZXZhilin Xu
Zhilin Xu
Objective This study explored the feasibility of mesoplasty with end-to-side anastomosis in the treatment of different apple-peel mesenteric defects with high jejunal atresia. Methods A retrospective analysis was performed on 42 premature infants admitted to the hospital between 2014 and 2021. Prenatal ultrasound scans revealed bowel dilatation. The patients experienced vomiting after birth and produced white or no meconium. Plain radiography showed double or triple bubble signs and the patients underwent emergency laparotomies. High jejunal atresia with different apple-peel atresia appearance was discovered intraoperatively, involving mobilization of the ileocecal region. Patients received end-to-side anastomosis between the enlarged blind pouch and atresic bowel, as well as mesoplasty. A jejunal feeding tube was placed trans-nasally. Patients were discharged after achieving full enteral feeding. Results Three patients died and 39 survived. The discharged patients were followed up for 12 months, and none showed post-operative complications such as intestinal obstruction, malnutrition, or chronic diarrhea. All surviving patients reached the expected height and weight for children of the same age. Conclusion For cases of high jejunal atresia with apple-peel intestinal atresia, mesoplasty is a good option to avoid postoperative volvulus.

3 April 2026 in Cell & Bioscience
Verified
Journal Article
Open access
PDF file
TYTing Yao
Ting Yao
MFMeili Fan
Meili Fan
ZHZenghui Hao
Zenghui Hao
ZJZaiqun Jiang
Zaiqun Jiang
XLXu Li
Xu Li
ZXZhilin Xu
Zhilin Xu
Hirschsprung’s disease (HSCR) is a congenital disorder characterized by intestinal aganglionosis. Despite evidence linking gut microbiota and immune