About

Li-Qing Chen is an Associate Professor in Plant Biology and also affiliated with the Center for Digital Agriculture and the National Center for Supercomputing Applications (NCSA) at the University of Illinois. Additionally, Chen is an affiliate of the Carl R. Woese Institute for Genomic Biology. Chen completed a Ph.D. at China Agricultural University and conducted postdoctoral research at the Carnegie Institution for Science in the Department of Plant Biology at Stanford, CA. Chen's research focuses on the control of sugar allocation in plants to improve crop yield and biomass production for food and biofuels. This work is essential for advancing a sustainable bio-based economy aimed at enhancing global food security and reducing dependence on fossil fuels for energy and industrial raw materials. Chen's core interest lies in unraveling the regulatory networks that control and coordinate the allocation of photoassimilates, primarily sugars produced in mature leaves, to various plant sinks such as roots, fruits, and seeds. Despite decades of research on carbon allocation and sugar translocation, these regulatory networks remain largely elusive. To address this, Chen employs a combination of in vivo biochemistry, cell biology, molecular genetics, systems biology, and synthetic biology to engineer and optimize assimilate allocation in plants.

Research topics

• Medicine
• Biochemistry
• Endocrinology
• Biology
• Cell biology
• Cancer research
• Chemistry
• Internal medicine
• Immunology
• Genetics

Selected publications

• FXR and BET signaling orchestrate to protect β cells

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-04-14

  articleOpen access

  Abstract In both type 1 and type 2 diabetes (T1D and T2D), insulin-producing β cells undergo progressive dysfunction due to inflammation, leading to impaired glucose responsiveness, dedifferentiation, and cell loss. While bile acid (BA) dysregulation under diabetic conditions is known to influence metabolic and inflammatory pathways, its mechanistic role in β cell regulation remains incompletely defined 1–3 . Here we show that bile acid sensor Farnesoid X receptor (FXR) and Bromodomain and Extra-Terminal motif (BET) signaling cooperatively regulates β cell inflammatory response and β cell identity. We identified the physiological protein-protein interaction between FXR and the bromodomain-containing protein 4 (BRD4) as a regulatory axis that protects against β cell dysfunction. We show that FXR activation by Fexaramine (Fex) together with BRD4 inhibition by JQ1 synergistically suppressed IL-1β-induced inflammation while also improving β cell identity and insulin secretion in both db/db model and high-fat diet (HFD) plus multi low-dose streptozotocin (MLD-STZ) model of diabetes. Importantly, this cooperative effect is abolished in β cell–specific FXR knockout (βFXRKO) mice, establishing that FXR is required for the functional synergy between these pathways in vivo . Mechanistically, structure-guided modeling and mutational analyses identified a direct interaction between FXR and the BD2 domain of BRD4, depending on specific lysine acetylation sites. Additionally, inhibition of the BD2 domain of BET combined with FXR activation markedly improved β cell survival in human T1D and T2D models established from human pluripotent stem cell (hPSC)-derived islet-like organoids (HILOs). Collectively, these findings establish a BA–bromodomain axis as a transcriptional interface linking metabolic signaling and chromatin regulation, and highlight FXR–BET targeting as a promising strategy to counter progressive β cell failure in diabetes.

  PublisherDOI

• Anti‐Aging Protein Klotho Attenuates Schizophrenia‐Associated Cognitive and Synaptic Dysfunctions by Regulating GluN2B‐NMDARs in the Hippocampus

  Journal of Neurochemistry · 2026-05-01

  article

  Cognitive impairment is a core symptom of schizophrenia and has a significant impact on clinical efficacy and prognosis. However, its underlying pathological mechanism remains unclear and effective treatments are still lacking. N-methyl-D-aspartate receptors (NMDARs) hypofunction is the key pathological basis of cognitive impairments in schizophrenia and the anti-aging protein klotho is involved in the regulation of NMDAR function. Our current study aims to investigate the role of klotho in synaptic and cognitive function in a male rat model of schizophrenia, in which rats are briefly exposed to dizocilpine (MK-801) to disrupt NMDAR during early development. We found that MK-801 treatment resulted in hippocampus-dependent synaptic plasticity and cognitive deficits in male rats during adulthood, and the expression of klotho protein in the hippocampus was significantly decreased in these rats. Elevation of hippocampal klotho in MK-801-treated rats via gene overexpression can significantly reverse the synaptic and cognitive dysfunction. At the molecular level, elevation of hippocampal klotho selectively upregulated the total and synaptic expressions of GluN2B-containing NMDARs, significantly increased postsynaptic density protein 95 (PSD-95) level and promoted extracellular signal-regulated kinase (ERK) phosphorylation in the hippocampus of MK-801-treated rats. Furthermore, treatment with a specific GluN2B antagonist Ro 25-6981 significantly abolished the beneficial effects of klotho on hippocampal long-term potentiation (LTP) and cognition in MK-801-treated rats. Collectively, reduced klotho in the hippocampus may contribute to the development of MK-801-induced schizophrenia-like synaptic and cognitive deficits, and elevating klotho is capable of rescuing the synaptic plasticity and cognition by modulating hippocampal GluN2B-containing NMDARs.

  PublisherDOI

• Human collagen III mRNA therapy for effective skin rejuvenation

  Journal of Translational Medicine · 2025-11-13

  articleOpen access

  BACKGROUND: Skin photoaging leads to the deterioration of dermal collagen and overall skin integrity, resulting in visible signs of aging, particularly around the eye. Collagen III plays a pivotal role in maintaining skin elasticity and facilitating proper collagen fibril organization. Messenger RNA (mRNA)-based therapeutics present a novel alternative for addressing these limitations by enabling the localized production of full-length, biologically active proteins. METHODS: This study evaluates the therapeutic effects of human collagen III (hCOL3A1) mRNA on UVB-induced skin photoaging using in vitro and in vivo models. In vitro, human fibroblasts were used to assess oxidative stress, senescence, apoptosis, proliferation, and migration. In vivo, a UVB-induced murine photoaging model was used to assess skin barrier function, dermal thickness, collagen content, and senescence markers were analyzed post-treatment. Transcriptome analysis was conducted to explore gene expression changes and key pathways involved in photoaging and repair mechanisms. RESULTS: Our findings demonstrate that hCOL3A1 mRNA reduces oxidative stress, senescence, apoptosis and promotes cell proliferation and migration in a photoaging cell model. In a murine photoaging model, hCOL3A1 mRNA significantly improves skin barrier function, enhances dermal thickness, restores collagen content, improves dermal structure, and reduces cellular senescence markers without inducing systemic toxicity or immunogenicity. Transcriptome analyses reveal that hCOL3A1 mRNA reverses UVB-induced gene expression changes, reinstating critical signaling pathways for skin homeostasis and fibroblast function. CONCLUSIONS: These results highlight hCOL3A1 mRNA as a promising therapeutic candidate for skin photoaging and underscore the potential of mRNA-based therapies in dermatology and regenerative medicine.

  PublisherOA PDFDOI

• Abstract 2131 H. pylori upregulates PD-L1 expression for immune evasion via mTOR ubiquitination and activation

  Journal of Biological Chemistry · 2025-05-01

  articleOpen accessSenior author

  Helicobacter pylori (H. pylori) is a human pathogen that colonizes the stomach of more than half of the population. The infected host is unable to clear the bacteria even with the induction of innate and adaptive immune responses. Persistent H. pylori infection is the leading cause of chronic gastritis, peptic ulcer disease and gastric cancer. Virulence factors of H. pylori play an important role in the pathogenicity of H. pylori infection. The cytotoxin-associated gene A (CagA) protein of H. pylori is delivered into the host gastric epithelial cells by bacterial type IV secretion system (T4SS) and hijacks host signaling molecules to promotes neoplastic transformation of gastric epithelial cells.

  PublisherOA PDFDOI

• Deep generative optimization of mRNA codon sequences for enhanced mRNA translation and therapeutic efficacy

  Nature Communications · 2025-11-12 · 10 citations

  articleOpen access

  Messenger RNA (mRNA) therapeutics show immense promise, but their efficacy is limited by suboptimal protein expression. Here, we present RiboDecode, a deep learning framework that generates mRNA codon sequences for enhanced mRNA translation. RiboDecode introduces several advances, including direct learning from large-scale ribosome profiling data and generative exploration of a large sequence space. In silico analysis demonstrates RiboDecode’s robust predictive accuracy for unseen genes and cellular environments. In vitro experiments showed substantial improvements in protein expression, significantly outperforming past methods. In addition, RiboDecode enables mRNA design with consideration of cellular context and demonstrates robust performance across different mRNA formats, including m1Ψ-modified and circular mRNAs, an important feature for mRNA therapeutics. In vivo mouse studies showed that optimized influenza hemagglutinin mRNAs induce ten times stronger neutralizing antibody responses against influenza virus compared to the unoptimized sequence. In an optic nerve crush model, optimized nerve growth factor mRNAs achieve equivalent neuroprotection of retinal ganglion cells at one-fifth the dose of the unoptimized sequence. Collectively, RiboDecode represents a paradigm shift from rule-based to a data-driven, context-aware approach for mRNA therapeutic applications, enabling the development of more potent and dose-efficient treatments. Messenger RNA therapeutics hold great promise but are limited by suboptimal protein expression. Here, the authors develop RiboDecode, a deep learning framework that generates optimized mRNA codon sequences to significantly enhance translation efficiency and therapeutic efficacy in both vaccines and protein replacement therapies.

  PublisherOA PDFDOI

• Molecular mechanisms linking adipose tissue-derived small extracellular vesicles/exosomes to the development or amelioration of obesity, insulin resistance, and diabetes-related complications

  European journal of medical research · 2025-10-31 · 6 citations

  reviewOpen access1st author

  Diabetes mellitus (DM) is a chronic metabolic disorder characterized by impaired glucose storage and utilization in adipose tissue and skeletal muscle. Type 2 diabetes mellitus (T2DM) is particularly prevalent among individuals with obesity, as excess weight fosters significant health complications, including inflammation and insulin resistance, ultimately contributing to the development of T2DM. It is believed that the crosstalk between adipose tissue, skeletal muscle, and the endocrine pancreas underlies the glucose dysmetabolism associated with excess weight. Extracellular vesicles (EVs) can play a role in mediating intercellular crosstalk and could be involved in the pathogenesis of T2DM and related complications in individuals with obesity. Exosomes/small EVs (sEVs) derived from adipose tissue may contribute to either the progression or management of metabolic syndromes, primarily through their effects on insulin resistance. Hence, the current narrative review was designed to evaluate the effect of adipose-derived sEVs in insulin resistance and its related complications. These sEVs have been isolated from white adipose tissue (WAT), brown adipose tissue (BAT), adipose-derived stem cells (ADSCs), adipose tissue macrophages (ATMs), as well as from plasma and other tissues of obese individuals and animal models. The present review showed that sEVs derived from adipose tissue and/or obese individuals and animal models may contribute significantly to the onset and enhancement of insulin resistance. However, sEVs extracted from ADSCs of healthy adipose tissue could enhance insulin sensitivity via their bioactive components (e.g., microRNAs). Additional complementary studies are required to validate the dual role of adipose-derived sEVs on the amelioration or progression of insulin resistance-related complications.

  PublisherOA PDFDOI

• BRD4 regulates PAI-1 expression in tumor-associated macrophages to drive chemoresistance in colorectal cancer

  Oncogene · 2025-05-28 · 8 citations

  article
  PublisherDOI

• Association between sleep duration and possible sarcopenia in middle-aged and elderly Chinese individuals: evidence from the China health and retirement longitudinal study

  BMC Geriatrics · 2024-07-11 · 20 citations

  articleOpen access1st author

  BACKGROUND: Sarcopenia is a common cause of disability in the aging population, and managing sarcopenia is an important step in building intrinsic capacity and promoting healthy aging. A growing body of evidence suggests that sleep deprivation may be a mediator of the development of sarcopenia. The purpose of this study was to explore the longitudinal association between sleep duration and possible sarcopenia using data from a national sample. METHODS: Two waves of data from the CHARLS database for 2011 and 2015 were used in this study. All possible sarcopenia participants met the Asia Working Group for Sarcopenia 2019 (AWGS 2019) diagnostic criteria. Sleep duration was assessed using a self-report questionnaire, and sleep duration was categorized as short (≤ 6 h), medium (6-8 h), or long (> 8 h) based on previous studies. Longitudinal associations between sleep duration and possible sarcopenia will be calculated by univariate and multifactorial logistic regression analyses and expressed as odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: A total of 5654 individuals participated in the follow-up study, with a prevalence of possible sarcopenia of 53.72% (578) in the short sleep duration group, 38.29% (412) in the medium sleep duration group, and 7.99% (86) in the long sleep duration group. According to the crude model of the second-wave follow-up study, short sleep durations were significantly more strongly associated with possible sarcopenia than were medium and long sleep durations (OR: 1.35, 95% CI: 1.17-1.55, P = 0.000). The association between short sleep duration and possible sarcopenia was maintained even after adjustment for covariates such as age, gender, residence, education level, BMI, smoking status, alcohol consumption and comorbidities (OR: 1.18, 95% CI: 1.02-1.36, P = 0.029). In the subgroup analysis, short sleep duration was associated with low grip strength (OR: 1.20, 95% CI: 1.02-1.41, P = 0.031). CONCLUSIONS: Sleep deprivation may be closely associated with the development of possible sarcopenia in middle-aged and elderly people, which provides new insights and ideas for sarcopenia intervention, and further studies are needed to reveal the underlying mechanisms involved.

  PublisherOA PDFDOI

• Deep Generative Optimization of mRNA Codon Sequences for Enhanced mRNA Translation and Therapeutic Efficacy

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-09-08 · 9 citations

  preprint

  ABSTRACT Messenger RNA (mRNA) therapeutics show immense promise, but their efficacy is limited by suboptimal protein expression. Here, we present RiboDecode, a deep learning framework that generates mRNA codon sequences for enhanced mRNA translation. RiboDecode introduces several advances, including direct learning from large-scale ribosome profiling data and generative exploration of a large sequence space. In silico analysis demonstrates RiboDecode’ s robust predictive accuracy for unseen genes and cellular environments. In vitro experiments showed substantial improvements in protein expression, significantly outperforming past methods. In addition, RiboDecode enables mRNA design with consideration of cellular context and demonstrates robust performance across different mRNA formats, including m 1 Ψ-modified and circular mRNAs, an important feature for mRNA therapeutics. In vivo mouse studies showed that optimized influenza hemagglutinin mRNAs induce ten times stronger neutralizing antibody responses against influenza virus compared to the unoptimized sequence. In an optic nerve crush model, optimized nerve growth factor mRNAs achieve equivalent neuroprotection of retinal ganglion cells at one-fifth the dose of the unoptimized sequence. Collectively, RiboDecode represents a paradigm shift from rule-based to a data-driven, context-aware approach for mRNA therapeutic applications, enabling the development of more potent and dose-efficient treatments.

  PublisherDOI

• Sleep duration and leisure activities are involved in regulating the association of depressive symptoms, muscle strength, physical function and mild cognitive impairment

  Heliyon · 2024-06-27 · 8 citations

  articleOpen access1st authorCorresponding

  <h2>Abstract</h2><h3>Background</h3> In order to lessen the burden of Alzheimer's disease (AD), timely and efficient management and intervention methods for mild cognitive impairment (MCI) are crucial. MCI is seen as a transitional stage between normal aging and dementia. Although sarcopenia is an important risk factor for MCI, it is unclear what factors mediates and regulates the brain-muscle communication. Our objective was to investigate the indirect moderating effects of sleep duration and leisure activity on depressive symptoms, sarcopenia and MCI. <h3>Method</h3> Panel data from the 2015 China Health and Retirement Longitudinal Study (CHARLS) database was used in this investigation. we used Bootstrap sampling to determine the relationship between sleep duration, leisure activity, depressive symptoms, sarcopenia, and MCI in mediation and indirect moderation models. The outcome measurements were odds ratio (OR) and confidence interval (CI). <h3>Result</h3> After adjusting for confounding variables, we discovered that sarcopenia and its traits, such as handgrip strength, gait speed, standing test, and muscle mass, were significantly correlated with MCI. Second, the results implied that depressive symptoms played a role in modulating the link between physical function, muscle strength, and MCI. This moderating effect was impacted by short sleep duration and moderate to high levels of leisure activities. <h3>Conclusion</h3> We discovered that MCI was highly correlated not only with physical function and muscle strength but also with depressed symptoms, which acted as a partially mediating factor in this connection. Handgrip strength, gait speed, and standing test mediated the correction of MCI caused by depression symptoms. Importantly, leisure activities and sleep duration had indirect moderating effects on the above associations, and future management policies should take these factors into account.

  PublisherDOI

Recent grants

• Inactivation of RUNX3 by Helicobacter pylori and gastric cancer

  NIH · $398k · 2012–2015

• NF-kB Signaling and H. Pylori-induced Gastric Disease

  NIH · $1.6M · 2010–2016

• Transcriptional regulation of H. pylori-mediated gastric inflammation and cancer

  NIH · $446k · 2013–2017

• Antimicrobial activity of pH-activated polypeptides toward H. pylori

  NIH · $436k · 2015–2017

Frequent coauthors

• Warner C. Greene

  Gladstone Institutes

  29 shared

• Margaret A. Shipp

  Dana-Farber Cancer Institute

  16 shared

• Xiaodong Yang

  14 shared

• Yoshiaki Ito

  13 shared

• Acacia Lamb

  Children's Hospital of The King's Daughters

  12 shared

• Eefjan Breukink

  Utrecht University

  11 shared

• Ben Berkhout

  Amsterdam University Medical Centers

  11 shared

• Pimchai Chaiyen

  11 shared

Labs

• Chen LabPI

  Not provided

Education

• PhD, School of Medicine

  Kyoto University

  1999