Sheng jianpeng

Prof. Sheng jianpeng


Research Focus & Metrics

Academic Career Length

6Years (2021-Present)

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

Representative Publications

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21 June 2023 in Nature Communications
Verified
Journal Article
Open access
PDF file
JDJuan Du
Juan Du
JZJunlei Zhang
Junlei Zhang
LWLin Wang
Lin Wang
XWXun Wang
Xun Wang
YZYaxing Zhao
Yaxing Zhao
SJSheng jianpeng
Sheng jianpeng
Ulcerative colitis is a chronic inflammatory bowel disorder with cellular heterogeneity. To understand the composition and spatial changes of the ulcerative colitis ecosystem, here we use imaging mass cytometry and single-cell RNA sequencing to depict the single-cell landscape of the human colon ecosystem. We find tissue topological changes featured with macrophage disappearance reaction in the ulcerative colitis region, occurring only for tissue-resident macrophages. Reactive oxygen species levels are higher in the ulcerative colitis region, but reactive oxygen species scavenging enzyme SOD2 is barely detected in resident macrophages, resulting in distinct reactive oxygen species vulnerability for inflammatory macrophages and resident macrophages. Inflammatory macrophages replace resident macrophages and cause a spatial shift of TNF production during ulcerative colitis via a cytokine production network formed with T and B cells. Our study suggests components of a mechanism for the observed macrophage disappearance reaction of resident macrophages, providing mechanistic hints for macrophage disappearance reaction in other inflammation or infection situations.

20 May 2022 in Cancer Immunology Research
Verified
Journal Article
Closed access
PDF file
XBXuanwen Bao
Xuanwen Bao
QLQiong Li
Qiong Li
JCJinzhang Chen
Jinzhang Chen
DCDiyu Chen
Diyu Chen
CYChanqi Ye
Chanqi Ye
Jian RuanJian Ruan
Jian Ruan
Intrahepatic cholangiocarcinoma (ICC) is a relatively rare but highly aggressive tumor type that responds poorly to chemotherapy and immunotherapy. Comprehensive molecular characterization of ICC is essential for the development of novel therapeutics. Here, we constructed two independent cohorts from two clinic centers. A comprehensive multiomics analysis of ICC via proteomic, whole-exome sequencing (WES), and single-cell RNA sequencing (scRNA-seq) was performed. Novel ICC tumor subtypes were derived in the training cohort (n = 110) using proteomic signatures and their associated activated pathways, which were further validated in a validation cohort (n = 41). Three molecular subtypes, chromatin remodeling, metabolism, and chronic inflammation, with distinct prognoses in ICC were identified. The chronic inflammation subtype was associated with a poor prognosis. Our random forest algorithm revealed that mutation of lysine methyltransferase 2D (KMT2D) frequently occurred in the metabolism subtype and was associated with lower inflammatory activity. scRNA-seq further identified an APOE+C1QB+ macrophage subtype, which showed the capacity to reshape the chronic inflammation subtype and contribute to a poor prognosis in ICC. Altogether, with single-cell transcriptome-assisted multiomics analysis, we identified novel molecular subtypes of ICC and validated APOE+C1QB+ tumor-associated macrophages as potential immunotherapy targets against ICC.

19 March 2024 in Drug Resistance Updates
Verified
Journal Article
Closed access
GCGang Che
Gang Che
JYJie Yin
Jie Yin
WWWankun Wang
Wankun Wang
YLYandong Luo
Yandong Luo
YCYiran Chen
Yiran Chen
JLJian Liu
Jian Liu

5 August 2024 in Nature Nanotechnology
Verified
Journal Article
Closed access
PDF file
XHXi Hu
Xi Hu
BZBo Zhang
Bo Zhang
MZMiao Zhang
Miao Zhang
WLWenshi Liang
Wenshi Liang
BHBangzhen Hong
Bangzhen Hong
Daishun LingDaishun Ling
Daishun Ling

14 February 2021 in Angewandte Chemie International Edition
Verified
Journal Article
Closed access
PDF file
BWBaiheng Wu
Baiheng Wu
ZSZhu Sun
Zhu Sun
JWJiangchao Wu
Jiangchao Wu
JRJian Ruan
Jian Ruan
PZPeng Zhao
Peng Zhao
Dong ChenDong Chen
Dong Chen

6 June 2023 in Cell Reports
Verified
Journal Article
Open access
JZJunlei Zhang
Junlei Zhang
JSJinyuan Song
Jinyuan Song
STShima Tang
Shima Tang
YZYaxing Zhao
Yaxing Zhao
LWLin Wang
Lin Wang
XBXueli Bai
Xueli Bai
Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal cancer that typically demonstrates resistance to chemotherapy. Tumor-associated macrophages (TAMs) are essential in tumor microenvironment (TME) regulation, including promoting chemoresistance. However, the specific TAM subset and mechanisms behind this promotion remain unclear. We employ multi-omics strategies, including single-cell RNA sequencing (scRNA-seq), transcriptomics, multicolor immunohistochemistry (mIHC), flow cytometry, and metabolomics, to analyze chemotherapy-treated samples from both humans and mice. We identify four major TAM subsets within PDAC, among which proliferating resident macrophages (proliferating rMφs) are strongly associated with poor clinical outcomes. These macrophages are able to survive chemotherapy by producing more deoxycytidine (dC) and fewer dC kinases (dCKs) to decrease the absorption of gemcitabine. Moreover, proliferating rMφs promote fibrosis and immunosuppression in PDAC. Eliminating them in the transgenic mouse model alleviates fibrosis and immunosuppression, thereby re-sensitizing PDAC to chemotherapy. Consequently, targeting proliferating rMφs may become a potential treatment strategy for PDAC to enhance chemotherapy.