Ting Pan
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Ting Pan has a total of 21 co-authors. Here are the top co-authors by number of shared publications:
- Bin Zhou
CAS CEMCS-CUHK Joint Laboratory, New Cornerstone Science Laboratory, Key Laboratory of Multi-Cell Systems, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China
1 shared publication - Cheng Dong
Department of Biochemistry and Molecular Biology, Tianjin Medical University, Tianjin 300070, People's Republic of China
1 shared publication - Dandan Huang
Department of Pharmacology, State Key Laboratory of Experimental Hematology, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Tianjin Key Laboratory of Inflammation Biology, School of Basic Medical Sciences, Tianjin Medical University , Tianjin 300070
1 shared publication Danyang Tian
Department of Pharmacology, Tianjin Key Laboratory of Inflammatory Biology, Center for Cardiovascular Diseases, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-Sponsored Collaborative Innovation Center for Medical Epigenetics, State Key Laboratory of Experimental Hematology (S.G., T.P., Y.C., R.D., Q.L., Y. Zhuo, Y. Zhao, D.T., X.S., T.Q., X.C., D.H., Y.S., Y.Y.), School of Basic Medical Sciences, Tianjin Medical University, China
1 shared publication- Jiong-Wei Wang
Department of Surgery, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore
1 shared publication Qian Liu
Department of Pharmacology, Tianjin Key Laboratory of Inflammatory Biology, Center for Cardiovascular Diseases, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-Sponsored Collaborative Innovation Center for Medical Epigenetics, State Key Laboratory of Experimental Hematology (S.G., T.P., Y.C., R.D., Q.L., Y. Zhuo, Y. Zhao, D.T., X.S., T.Q., X.C., D.H., Y.S., Y.Y.), School of Basic Medical Sciences, Tianjin Medical University, China
1 shared publication
Latest Publications
- 30 January 2026
- Published by Wolters Kluwer Health in Circulation Research
- Vol. 138 (3)
Differential Impact of Recruited and Resident Macrophages on Hypoxia-Induced Pulmonary Hypertension
BACKGROUND: Pulmonary interstitial macrophages can be divided into 2 distinct subsets with different origins: resident macrophages (resMФs) and recruited macrophages (recMФs). However, their specific roles in pulmonary arterial hypertension remain unclear. METHODS: Bone marrow transplantation, the DT (diphtheria toxin) receptor system, and genetically modified murine models were utilized to explore how key TFs (transcription factors) regulate phenotype alterations in pulmonary resMФs and recMФs in an SU5416/hypoxia murine model of pulmonary hypertension (PH). Therapeutic approaches included DNA aptamer–based proteolysis-targeting chimera and small interfering RNA–loaded lipid nanoparticle for treating SU5416/hypoxia–exposed rats. RESULTS: Depletion of either resMФs or recMФs using DT treatment significantly reduced SU5416/hypoxia–induced PH in mice. Pulmonary recMФs exhibited a proinflammatory phenotype during PH, driven by the TF Hic1 (hypermethylated in cancer 1). Bone marrow transplantation with Hic1 −/− recMФs ameliorated PH in mice. Hic1 enhanced proinflammatory gene transcription by inhibiting Sirt1 (sirtuin 1)-mediated H3K9ac (histone H3 lysine 9 acetylation) deacetylation in the promoter regions. In contrast, pulmonary resMФs demonstrated a profibrotic transcriptome characterized by upregulation of MMP genes that are, in turn, regulated by Prrx2 (paired-related homeobox 2). Prrx2 deletion in resMФs protected against PH in mice by reducing perivascular fibrosis. Simultaneously targeting Prrx2 and Hic1 in macrophages significantly alleviated SU5416/hypoxia–induced PH in rats. CONCLUSIONS: The differential roles of pulmonary resMФs and recMФs in pulmonary vascular remodeling highlight novel therapeutic targets for pulmonary arterial hypertension treatment, specifically through inhibition of Hic1 and Prrx2 in macrophages.
- 30 January 2026
- Published by Wolters Kluwer Health in Circulation Research
- Vol. 138 (3)
Differential Impact of Recruited and Resident Macrophages on Hypoxia-Induced Pulmonary Hypertension
BACKGROUND: Pulmonary interstitial macrophages can be divided into 2 distinct subsets with different origins: resident macrophages (resMФs) and recruited macrophages (recMФs). However, their specific roles in pulmonary arterial hypertension remain unclear. METHODS: Bone marrow transplantation, the DT (diphtheria toxin) receptor system, and genetically modified murine models were utilized to explore how key TFs (transcription factors) regulate phenotype alterations in pulmonary resMФs and recMФs in an SU5416/hypoxia murine model of pulmonary hypertension (PH). Therapeutic approaches included DNA aptamer–based proteolysis-targeting chimera and small interfering RNA–loaded lipid nanoparticle for treating SU5416/hypoxia–exposed rats. RESULTS: Depletion of either resMФs or recMФs using DT treatment significantly reduced SU5416/hypoxia–induced PH in mice. Pulmonary recMФs exhibited a proinflammatory phenotype during PH, driven by the TF Hic1 (hypermethylated in cancer 1). Bone marrow transplantation with Hic1 −/− recMФs ameliorated PH in mice. Hic1 enhanced proinflammatory gene transcription by inhibiting Sirt1 (sirtuin 1)-mediated H3K9ac (histone H3 lysine 9 acetylation) deacetylation in the promoter regions. In contrast, pulmonary resMФs demonstrated a profibrotic transcriptome characterized by upregulation of MMP genes that are, in turn, regulated by Prrx2 (paired-related homeobox 2). Prrx2 deletion in resMФs protected against PH in mice by reducing perivascular fibrosis. Simultaneously targeting Prrx2 and Hic1 in macrophages significantly alleviated SU5416/hypoxia–induced PH in rats. CONCLUSIONS: The differential roles of pulmonary resMФs and recMФs in pulmonary vascular remodeling highlight novel therapeutic targets for pulmonary arterial hypertension treatment, specifically through inhibition of Hic1 and Prrx2 in macrophages.