About

Hong Wang is a Professor of Mathematics at New York University. She has received notable awards including the 2025 Ostrowski Prize, the 2025 Salem Prize, and the 2025 ICCM Gold Medal of Mathematics, recognizing her significant contributions to the fields of harmonic analysis and geometric measure theory. Her work has been acknowledged for solving major open problems in these areas, and she is celebrated for her outstanding achievements in pure and applied mathematics, particularly among mathematicians of Chinese descent under the age of 45.

Research topics

• Biology
• Biochemistry
• Immunology
• Cell biology
• Microbiology
• Medicine
• Neuroscience
• Internal medicine
• Chemistry

Selected publications

• Repurposing a detrimental antibody epitope as targeted therapeutics for sepsis and rheumatoid arthritis

  Military Medical Research · 2026-02-17 · 2 citations

  articleOpen accessSenior authorCorresponding

  Background: Sepsis and rheumatoid arthritis (RA) are distinct yet mechanistically related conditions commonly driven by dysregulated inflammatory responses. Here, we explored the counterintuitive hypothesis that an epitope from a deleterious anti-tetranectin (TN) antibody (mAb9) could hold unforeseen therapeutic potential. Methods: By mapping mAb9's epitope to P2 (residues 55-70), a region crucial for TN's protective functions, we developed P2-1, a water-soluble derivative as a targeted therapy. We then employed animal models of sepsis (cecal ligation and puncture) and arthritis (collagen antibody-induced arthritis) to evaluate the therapeutic effects of P2, P2-1, and a procathepsin L (pCTS-L)-neutralizing antibody by assessing septic survival, arthritis severity, pain sensitivity, and joint tissue histology. In parallel, we utilized a surface plasmon resonance (SPR) assay and computational modeling to examine the P2-1/high mobility group box 1 (HMGB1) interaction. Finally, we elucidate the effect of P2-1 on the HMGB1-induced release of pCTS-L and other cytokines and chemokines using primary human peripheral blood mononuclear cells (PBMCs). Results: ) mRNA upregulation and pCTS-L secretion from human immune cells, crucially without perturbing other HMGB1-induced cytokines and chemokines. We further validated pCTS-L as a therapeutic target by demonstrating that a neutralizing antibody conferred potent antiarthritic effects, reducing joint inflammation, pain, and structural damage. Conclusions: Our findings introduce a paradigm-shifting drug discovery strategy that transforms insights from harmful antibody action into targeted therapeutics for the HMGB1-pCTS-L axis. This approach not only delivers P2-1 as a potent therapy but also establishes pCTS-L as a crucial mediator in inflammatory diseases such as sepsis and RA. Supplementary Information: The online version contains supplementary material available at 10.1186/s40779-026-00686-8.

  PublisherOA PDFDOI

• Additional file 1 of Repurposing a detrimental antibody epitope as targeted therapeutics for sepsis and rheumatoid arthritis

  Figshare · 2026-01-01

  articleOpen accessSenior author

  Additional file 1. Fig. S1 Modulation of HMGB1 extracellular functions through distinct molecular interactions. Fig. S2 Two representative full-range surface plasmon resonance (SPR) plots demonstrating the interaction between HMGB1 and P2-1. Fig. S3 Predicted P2 peptide structure and its docking interaction with HMGB1 B-box. Fig. 4 A tetranectin (TN) mutant lacking the N-terminal α-helix trimerization domain retained the protective efficacy of TN in sepsis. Fig. S5 Representative Cytokine Antibody Arrays depicting the effect of P2-1 on collagen antibody-induced arthritis (CAIA)-induced joint inflammation. Fig. S6 Prophylactic P2-1 treatment attenuated collagen antibody-induced arthritis (CAIA). Fig. S7 Volcano plots illustrating P2-1-modulated differential gene expression in HMGB1-stimulated human PBMCs. Fig. S8 Representative cytokine antibody arrays illustrating the effects of P2-1 on HMGB1-induced cytokines and chemokines. Fig. S9 Full Western blotting analysis of the effect of P2-1 on HMGB1-induced pCTS-L release in human PBMCs. Fig. S10 Representative cytokine antibody arrays illustrating the effect of mAb2 on collagen antibody-induced arthritis (CAIA)-induced joint inflammation. Fig. S11 Proposed model for P2-1-mediated intervention in the inflammatory HMGB1-pCTS-L axis in sepsis and rheumatoid arthritis. Table S1 Key reagent sources

  PublisherDOI

• Additional file 1 of Repurposing a detrimental antibody epitope as targeted therapeutics for sepsis and rheumatoid arthritis

  Figshare · 2026-01-01

  articleOpen accessSenior author

  Additional file 1. Fig. S1 Modulation of HMGB1 extracellular functions through distinct molecular interactions. Fig. S2 Two representative full-range surface plasmon resonance (SPR) plots demonstrating the interaction between HMGB1 and P2-1. Fig. S3 Predicted P2 peptide structure and its docking interaction with HMGB1 B-box. Fig. 4 A tetranectin (TN) mutant lacking the N-terminal α-helix trimerization domain retained the protective efficacy of TN in sepsis. Fig. S5 Representative Cytokine Antibody Arrays depicting the effect of P2-1 on collagen antibody-induced arthritis (CAIA)-induced joint inflammation. Fig. S6 Prophylactic P2-1 treatment attenuated collagen antibody-induced arthritis (CAIA). Fig. S7 Volcano plots illustrating P2-1-modulated differential gene expression in HMGB1-stimulated human PBMCs. Fig. S8 Representative cytokine antibody arrays illustrating the effects of P2-1 on HMGB1-induced cytokines and chemokines. Fig. S9 Full Western blotting analysis of the effect of P2-1 on HMGB1-induced pCTS-L release in human PBMCs. Fig. S10 Representative cytokine antibody arrays illustrating the effect of mAb2 on collagen antibody-induced arthritis (CAIA)-induced joint inflammation. Fig. S11 Proposed model for P2-1-mediated intervention in the inflammatory HMGB1-pCTS-L axis in sepsis and rheumatoid arthritis. Table S1 Key reagent sources

  PublisherDOI

• A neuroimmune pathway drives bacterial infection

  Science Advances · 2025-05-02 · 8 citations

  articleOpen access

  Pathogen-induced septic death presents a substantial public health challenge, with its neuroimmune mechanisms largely unexplored. Our study investigates neurotransmitter modulation of ACOD1 expression, a regulator of immunometabolism activated by bacterial lipopolysaccharide (LPS). Screening neurotransmitters identifies dopamine as a potent inhibitor of LPS-induced ACOD1 expression in innate immune cells. Mechanistically, DRD2 forms a complex with TLR4, initiating MAPK3-dependent CREB1 phosphorylation and subsequent ACOD1 transcription. Conversely, dopamine disrupts TLR4-MYD88 interaction via DRD2 without affecting the formation of the LPS-induced TLR4-MD2-CD14 complex. Enhanced ACOD1 expression induces CD274/PD-L1 production independently of itaconate, precipitating inflammation-associated immunosuppression in sepsis. Delayed administration of pramipexole, a dopamine agonist, mitigates lethality in bacterial sepsis mouse models. Conversely, the dopamine antagonist aripiprazole exacerbates sepsis mortality. Dysregulation of the dopamine-ACOD1 axis correlates with sepsis severity in patients, indicating a potential therapeutic target for modulating this neuroimmune pathway.

  PublisherDOI

• Correction: Plumbagin protects mice from lethal Sepsis by modulating immunometabolism upstream of PKM2

  Molecular Medicine · 2025-07-25

  erratumOpen access
  PublisherOA PDFDOI

• Echinacoside: A potential therapeutic approach for alcohol-related liver disease by alleviating intestinal microbial dysbiosis, intestinal barrier dysfunction, and liver inflammation mediated by the endotoxin-TLR4/NF-κB pathway

  European Journal of Pharmacology · 2025-07-30 · 2 citations

  article1st authorCorresponding
  PublisherDOI

• Pro-Dermcidin as an Emerging Regulator of Innate Immunity in Sepsis

  International Journal of Molecular Sciences · 2025-08-07 · 2 citations

  articleOpen accessSenior author

  Human dermcidin (DCD) is synthesized as a 110-amino acid precursor (pre-dermcidin, pre-DCD) containing a 19-residue leader signal sequence, which is removed to produce a leader-less pro-domain-containing peptide termed as pro-dermcidin, pro-DCD. Pro-DCD can be secreted by human eccrine sweat glands and then cleaved into antimicrobial peptides, such as dermcidin (DCD). Emerging evidence suggests that pro-DCD has broader physiological roles beyond antimicrobial defense, potentially serving as a therapeutic agent for inflammatory diseases like sepsis. In this review, we summarize recent evidence supporting pro-DCD as a regulator of innate immunity in sepsis.

  PublisherOA PDFDOI

• Repurposing a Detrimental Antibody Epitope as Targeted Therapeutics for Sepsis and Rheumatoid Arthritis.

  Research Square · 2025-09-19

  preprintOpen access1st authorCorresponding
  PublisherDOI

• Selective Trapping of In(III) Ions under σ-π* Bond Synergistic Effects by Modulating Lewis Basicity of Capture Sites on Nanofibers

  Langmuir · 2025-03-26

  articleSenior author

  Effectively selective recovery and separation of indium from alternative resources are of great environmental and economic significance. Although adsorption plays a critical role in this process, the design of highly selective capture sites remains a great challenge. Inspired by molecular orbital theory and hard and soft acids and bases theory (HSAB), we recognize that the nonequivalent orbital hybridization of In(III) ions renders them susceptible to deformation, exhibiting softer Lewis acidity. Herein, the thioacetamide-modified nanofiber (TAANF), with the O═C─NH─C═S as the capture sites, was prepared through an electrospinning technique combined with chemical modification. As expected, the O═C─NH─C═S exhibits softer Lewis basicity via modulated Lewis basicity of C═S by C═O, which better matches the Lewis acidity of In(III) ions to improve affinity. Adsorption studies showed that TAANF exhibited excellent properties for In(III) ions, especially in terms of selectivity; the selectivity coefficients range from 20 to 276 for K(I), Ca(II), Na(I), Mg(II), Mn(II), Zn(II), and Fe(II) ions in a multicomponent system. Furthermore, the capture mechanism indicates that In(III) ions not only can accept electrons from capture sites but also donate rich d2 orbit electrons to the π orbitals of capture sites, as demonstrated by XAFS, XPS, and DFT. This enables selective capture of In(III) ions by forming a stable six-membered ring under the synergistic effect of σ and feedback π bonds (σ-π*). Finally, this work provides a strategy to design highly selective capture sites and holds promise for recovering In(III) ions from alternative sources.

  PublisherDOI

• Polysaccharides from Cistanche deserticola Ma prevent alcoholic fatty liver disease by regulating hepatic lipid metabolism and gut microbiota in mice

  International Immunopharmacology · 2025-04-26 · 7 citations

  articleOpen access

  Cistanche deserticola Ma polysaccharide (CDP) is an active ingredient extracted from Cistanche deserticola Ma (CD) and is believed to have hepatoprotective activity. However, the molecular mechanism of its hepatoprotective effect by intervening in alcoholic fatty liver disease (AFLD) remains unclear. In the present study, three polysaccharides were isolated and purified from CD, and the polysaccharide with the better lipid-lowering and liver-protecting activity and the highest yield, CDPS, was selected by in vitro experiments for subsequent. The efficacy of CDPS in ameliorating AFLD in mice was evaluated using hepatic lipidomics, 16S rRNA analysis and molecular biology experiments. The present study showed that CDPS significantly improved alcohol-induced weight loss, lipid accumulation, ALT, AST, inflammation and dyslipidemia, suggesting that CDPS can prevent AFLD. Lipidomics showed that CDPS improved lipid metabolism disorders by regulating glycerophospholipid metabolism, linoleic acid metabolism, and arachidonic acid metabolism. 16S rRNA analysis showed that CDPS ameliorated alcohol-induced gut microbiota disruption. In particular, CDPS supplementation reduced the abundance of Bacteroides , Parabacteroides , and Escherichia-Shigella and increased the abundance of Ruminococcaceae_UCG-010 , Lachnospiraceae_NK4A136_group and Faecalibaculum abundance, and promoted the production of SCFAs. We further used Western blotting to determine the levels of proteins involved in lipogenesis and catabolism, and CDPS intervention resulted in decreased levels of lipid synthesis-associated proteins (SREBP-1c and FAS) and increased levels of lipid catabolism-associated proteins (PPARα) and p-AMPK/AMPK ratio. Our results suggest that CDPS has the potential to prevent AFLD by modulating lipid metabolism, altering the gut microbiota, increasing the content of SCFAs, activating the AMPK signaling pathway to promote fatty acid β-oxidation and limiting fatty acid biosynthesis, which provides a basis for further development of therapeutic drugs for AFLD. • In vitro screening of polysaccharides (CDPS) with the better lipid-lowering and hepatoprotective activities. • Preliminary characterization of CDPS as a heteropolysaccharide. • CDPS directly improves hepatic lipid metabolism through three metabolic pathways. • CDPS regulates the composition of intestinal flora reversing microbiota dysbiosis. • CDPS intervenes in AFLD mice by activating the AMPK signaling pathway.

  PublisherDOI

Recent grants

• Preclinical Development of a Novel Small Molecule Drug for Sepsis

  NIH · $333k · 2017–2019

• Mechanisms of Novel Herbal Therapies for Sepsis.

  NIH · $4.3M · 2010–2025

• NIH Grant R01GM070817

  NIH · $1.3M · 2009

• Cancer Research Career Enhancement and Related Activities

  NIH · $96.9M · 1997–2027

• Regulation of HMGB1 Release in Endotoxemia.

  NIH · $4.2M · 2002–2022

Frequent coauthors

• Kevin J. Tracey

  Feinstein Institute for Medical Research

  307 shared

• Shu Zhu

  Donald & Barbara Zucker School of Medicine at Hofstra/Northwell

  197 shared

• Ping Wang

  Southern University of Science and Technology

  164 shared

• Andrew E. Sama

  155 shared

• Jianhua Li

  Feinstein Institute for Medical Research

  141 shared

• Xiaoling Qiang

  Donald & Barbara Zucker School of Medicine at Hofstra/Northwell

  130 shared

• Wei Li

  Nanjing University of Chinese Medicine

  121 shared

• Guido Kroemer

  Assistance Publique – Hôpitaux de Paris

  117 shared

Education

• Ph.D., Microbiology

  Louisiana State University

  1992

• M.S., Microbiology

  Zhejiang University

  1987

• B.S., Biology

  Hebei University

  1984

Awards & honors

• Ostrowski Prize (2025)
• Salem Prize (2025)
• ICCM Gold Medal of Mathematics (2025)