About

Yi Lu is a professor in the Department of Bioengineering at the University of Illinois Urbana-Champaign. His primary research areas include bio-micro and nanotechnology, biomedical imaging, bioMEMS, biomolecular engineering, biomolecular modeling, biophotonics, biotechnology, cell and molecular engineering, chemical biosensors, drug delivery, environmental engineering, MRI, and scaffolding materials. His work focuses on developing micro/nano/molecular technologies in bioengineering, including novel molecular probes for bioimaging and targeted drug delivery agents for pharmaceutical applications. He is involved in advancing bioengineering research with an emphasis on innovative technologies for detecting and treating health issues.

Research topics

• Materials science
• Biology
• Nanotechnology
• Virology
• Genetics
• Computational biology
• Medicine

Selected publications

• 3-D-Printed Pentahedral Polarization-Division Transmissive Metadevice With Versatile Wavefronts

  IEEE Transactions on Antennas and Propagation · 2026-02-12 · 16 citations

  articleSenior author

  A novel pentahedral polarization-multiplexed metadevice concept is proposed via metasurfaces (MSs), providing an alternative avenue toward the capacity and versatility limit of integrated functions. First, a multi-layer anisotropic transmissive meta-atom is proposed for phase control of differently polarized waves. Next, five individual sub-MSs are designed and assembled using a 3D-printed pentahedral frame. Finally, a proof-of-concept pentahedral device is experimentally characterized, demonstrating diverse functionalities including the generation of highly directive beams, tri-beam radiation, dual-vortex beams, and dual-beam in orthogonal linearly polarized (LP) and decoupled co-/cross-circularly polarized (CP) channels. Measured and simulated results coincide well and illustrate the effectiveness of the space-polarization multiplexing concept in versatile wavefront control over a pentahedral platform.

  PublisherDOI

• Unraveling key genes and mitochondrial-related mechanisms of atherosclerosis severity: explorations based on interpretable machine learning

  BMC Cardiovascular Disorders · 2026-02-09

  articleOpen access

  Dysfunctional mitochondria increase oxidative stress and inflammation, driving atherosclerosis. Understanding gene expression and regulatory mechanisms is crucial. This study aims to identify key mitochondrial dysfunction-related genes (MitoDEGs) associated with atherosclerotic plaque severity, elucidate their molecular mechanisms and immune-regulatory roles in disease progression, and validate pivotal biomarkers to provide mechanistic insights for personalized therapeutic strategies. We utilized eight atherosclerotic plaque datasets (human samples) from GEO and mitochondrial gene data from MitoCarta3.0. Lasso Regression and the Shap algorithm were employed to identify key differentially expressed mitochondrial genes (MitoDEGs) for model construction. Enriched pathways were analyzed using GO and KEGG databases, and protein–protein interactions were explored with STRING and Cytoscape. Experimental validation was conducted using atherosclerosis mouse models and HUVEC cell models. This study identified distinct and shared mitochondrial dysfunction-related genes (MitoDEGs) in carotid and peripheral atherosclerotic plaques. Key carotid-specific MitoDEGs included HK3 and BID, while peripheral-specific ones included RAC2 and TCL1A. Two common MitoDEGs, GZMB and PMAIP1, were found in both plaque types. Enrichment analyses revealed novel associations with mitochondrial pathways including apoptosis, p53 signaling, hexose metabolism, and protein serine/threonine kinase regulation. Importantly, these MitoDEGs are mechanistically linked to mitochondrial outer membrane integrity and metabolic reprogramming. Experimental validation confirmed the upregulation of core MitoDEGs (CASP1, BID, PMAIP1, and GZMB), highlighting their critical roles in mitochondrial dysfunction during atherosclerosis progression. This study underscores the critical role of mitochondrial dysfunction, mediated by specific MitoDEGs, in atherosclerosis progression. The identified genes modulate both mitochondrial apoptotic pathways and immune cell infiltration, contributing to plaque severity. These shared and location-specific MitoDEGs offer novel mechanistic insights and represent potential therapeutic targets for intervening in plaque development and achieving personalized management of atherosclerotic disease.

  PublisherDOI

• Expected Insurance Coverage and Pharmaceutical Innovation: Evidence from China's National Drug Price Negotiation Policy

  SSRN Electronic Journal · 2026-01-01

  preprintOpen access
  PublisherDOI

• Inferring tumor immune microenvironment -related risk states from pretreatment H&E pathomics and clinical biomarkers to predict checkpoint inhibitor pneumonitis in advanced NSCLC: a multicenter multimodal study

  Frontiers in Immunology · 2026-02-19 · 1 citations

  articleOpen access

  Background: Checkpoint inhibitor pneumonitis (CIP) is a rare but potentially fatal immune-related adverse event (irAE) that can interrupt immune checkpoint blockade in non-small cell lung cancer (NSCLC). With no validated pretreatment biomarkers and a diagnosis largely made by exclusion, upfront risk stratification is required. Recent advances in artificial intelligence (AI)-driven pathomics have made it feasible to infer tumor immune microenvironment (TIME)-relevant risk states in patients with NSCLC. Accordingly, we leveraged hematoxylin and eosin(H&E)-based digital pathomics combined with clinical variables to interrogate the TIME in patients who developed CIP and to enable pretreatment and early prediction of CIP. Methods: In this retrospective study, 346 eligible patients from three hospitals were screened consecutively between January 2022 and January 2025. Patients were divided into CIP and non-CIP groups according to whether CIP occurred at a prespecified observation endpoint. We first developed a pathomics model that employed convolutional neural networks (CNNs) combined with multi-instance learning (MIL) to generate predictions at both the patch and whole slide image (WSI) levels on H&E-stained slides. Separately, we constructed a clinical model using logistic regression (LR) to process the structured clinical data accompanying each case. Subsequently, pathological and clinical information were integrated, where modeling was advanced from modality-specific feature learning to cross-modal representation learning, and final predictive modeling was completed. The predictive performance of different models was evaluated using the area under the Receiver Operating Characteristic (ROC) curve and benchmarked against unimodal models and standard ensemble methods. Results: When the models were evaluated across both internal validation and external test datasets, the pathomics model demonstrated noticeably stronger performance than the clinical approach, achieving area under the curve (AUC) scores of 0.916, 0.875(test 1), and 0.843(test 2), respectively, while the clinical model posted more modest results of 0.880, 0.569(test 1), and 0.594(test 2). The most significant outcome, however, emerged from the multimodal fusion model, which produced the strongest results of all, with performance metrics of 0.930, 0.919(test 1), and 0.905(test 2) in the validation and test phases, respectively. Conclusion: Pretreatment H&E-derived pathomics, integrated with baseline clinical biomarkers, enable accurate prediction of CIP risk in locally advanced or metastatic NSCLC. This framework supports proactive surveillance and individualized immune checkpoint inhibitor (ICI) strategies and provides a scalable route to decode TIME-relevant states from routine pathology.

  PublisherDOI

• Flavor dependence of chiral symmetry breaking and the conformal window

  Open MIND · 2026-02-16

  preprint

  We investigate the phase structure of Quantum Chromodynamics (QCD) in the vacuum as a function of quark flavor number $N_f$ within the chiral limit. By self-consistently solving the coupled DSEs for the quark and gluon propagators in a minimal QCD scheme, we elucidate the nonperturbative dynamics governing dynamical chiral symmetry breaking. Our calculations determine a critical flavor number of $N_f^c=6.81$ which marks the chiral symmetry restoration of quarks. Further analysis reveals the critical exponents of the chiral condensate as $ -\langle\barψ ψ\rangle\sim |N_f-N_f^c|^{0.53(9)}$, characterized the second order feature of this phase transition of chiral symmetry. Additionally, we discuss the implications for the walking regime towards the conformal window at larger flavor.

  DOI

• Flavor dependence of chiral symmetry breaking and the conformal window

  ArXiv.org · 2026-02-16

  articleOpen access

  We investigate the phase structure of Quantum Chromodynamics (QCD) in the vacuum as a function of quark flavor number $N_f$ within the chiral limit. By self-consistently solving the coupled DSEs for the quark and gluon propagators in a minimal QCD scheme, we elucidate the nonperturbative dynamics governing dynamical chiral symmetry breaking. Our calculations determine a critical flavor number of $N_f^c=6.81$ which marks the chiral symmetry restoration of quarks. Further analysis reveals the critical exponents of the chiral condensate as $ -\langle\barψ ψ\rangle\sim |N_f-N_f^c|^{0.53(9)}$, characterized the second order feature of this phase transition of chiral symmetry. Additionally, we discuss the implications for the walking regime towards the conformal window at larger flavor.

  PublisherOA PDF

• Screening natural raw materials and product development for improving insomnia based on network pharmacology and data mining

  Medicine · 2026-01-23

  articleOpen access

  Insomnia, as one of the most common sleep problems, seriously affects the normal life and work of individuals. Aromatherapy is regarded as a promising alternative medicine for improving sleep quality. Based on network pharmacology and data mining, this study screened natural raw materials for improving insomnia. Then, we developed an aromatherapy product informed by the screening results and investigated its mechanism for improving insomnia through network pharmacology. Five core insomnia targets were identified through literature. 1600 candidate compounds and 1757 candidate herbs related to the target were matched using HERB and TCMSP databases. By comparing with the Catalogue of Used Cosmetic Materials (2021 edition), 597 kinds of usable candidate materials were selected, including 85 raw materials related to target MTNR1A, 86 raw materials related to target MTNR1B, 120 raw materials related to target HTR1A, 7 raw materials related to target GABRB2, and 582 raw materials related to target GABRA1. Then based on the screening results, we selected sandalwood, lime, angelica sinensis, yilan, sage and lavender to design Pinghe Sleep Aromatherapy Product to improve insomnia. Network pharmacological analysis revealed that the main ingredients of the Pinghe Sleep Aromatherapy Product are beta-sitosterol, stigmasterol, isorhamnetin, luteolin, tanshinone IIA, D-limonene, and linalool. It exerts improvement effects by influencing targets such as IL6, TNF, AKT1, CASP3, TP53, and VEGFA, regulating signaling pathways such as AGE-RAGE, neuroactive ligand-receptor interactions, the HIF-1 signaling pathway, and the calcium signaling pathway. This study provides an idea of raw material screening and product development, which can save product development cost and shorten product development cycle by using network pharmacology and data mining.

  PublisherDOI

• Paradoxes in the Ontological Classification of Glia—Evidence for an Important New Class of Brain Cells with Primary Functions in Iron Regulation

  Cells · 2026-03-13

  articleOpen access

  The ontological categorization of the cellular elements of the brain was proposed over a century ago by Santiago Ramón y Cajal (neurons, astroglia) and Pío del Río-Hortega (oligodendroglia, microglia). It combines histochemical observations of morphology with allied inferences about the specialized functions and origins (ectoderm or mesoderm) of each cellular element. This ontology shapes modern neuroscience, with the main non-neuronal cells-astroglia, oligodendroglia and microglia-viewed as having distinct primary roles relating respectively to the metabolic support, myelination and immunoprotection of neurons, the information signaling cells. Yet contemporary techniques, ranging from electrophysiology to single-cell transcriptomics and ultrahigh resolution spectroscopy, are revealing intersecting molecular profiles and functional capacities of these cell groups, for example metabolic support, neuroimmune and signaling functions in oligodendroglia. Here we identify discrepancies in current glial paradigms, from empirical, evolutionary and pragmatic perspectives. We suggest a subset of small, iron-rich glial cells, usually with few processes, often viewed as oligodendroglia with myelin-related primary functions, instead have iron-related primary functions that are central to all aspects of brain activity. We call these 'ferriglia'. We discuss implications for pathogenesis across the spectrum of neuropsychiatric and neurological disorders, including neurodegenerative conditions such as Alzheimer's disease and other less common cognitive, movement and neurobehavioral disorders, stroke and cerebrovascular disease, glioblastoma and other brain cancers and neuroimmune conditions. We also briefly address the question of where ferriglia may reside within existing glial compartments and lineages, implications for the ontological classification of other glial cells, and research challenges that must be overcome going forward.

  PublisherOA PDFDOI

• Simultaneous Imaging of Cu ⁺ and Cu ² ⁺ in Neural Cells Using DNAzyme Probes Reveals Mechanistic Link Between Copper Redox Imbalance and Amyloid Pathology

  Angewandte Chemie · 2026-02-24

  articleSenior author

  ABSTRACT Copper dysregulation is implicated in neurodegenerative diseases such as Alzheimer's disease (AD), yet its precise role in neuronal death remains unclear. To address this issue, here, we introduce a pair of Cu + and Cu 2 + specific DNAzymes‐based fluorescent probes, for the first time, enabling simultaneous visualization of both redox states of copper in single living neurons. Using this dual‐color system, we found that amyloid‐beta (Aβ) oligomerization promotes intracellular copper accumulation, distinct from that induced by artificial ionophore loading. Elevated Cu + drives reactive oxygen species (ROS) generation, lipoylated protein aggregation, and FDX1‐dependent cuproptosis, while Cu + chelation or FDX1 knockdown completely prevents cell death. In contrast, ROS scavengers only partially rescue viability, demonstrating that neuronal death is driven by copper overload, not oxidative stress itself. These findings redefine the mechanistic framework linking copper redox imbalance to Aβ pathology and neuronal vulnerability and demonstrate a selective, sensitive approach for monitoring copper homeostasis and its disruption in neurodegenerative disease.

  PublisherDOI

• Simultaneous Imaging of Cu ⁺ and Cu ² ⁺ in Neural Cells Using DNAzyme Probes Reveals Mechanistic Link Between Copper Redox Imbalance and Amyloid Pathology

  Angewandte Chemie International Edition · 2026-02-21

  articleOpen accessSenior authorCorresponding

  ABSTRACT Copper dysregulation is implicated in neurodegenerative diseases such as Alzheimer's disease (AD), yet its precise role in neuronal death remains unclear. To address this issue, here, we introduce a pair of Cu + and Cu 2 + specific DNAzymes‐based fluorescent probes, for the first time, enabling simultaneous visualization of both redox states of copper in single living neurons. Using this dual‐color system, we found that amyloid‐beta (Aβ) oligomerization promotes intracellular copper accumulation, distinct from that induced by artificial ionophore loading. Elevated Cu + drives reactive oxygen species (ROS) generation, lipoylated protein aggregation, and FDX1‐dependent cuproptosis, while Cu + chelation or FDX1 knockdown completely prevents cell death. In contrast, ROS scavengers only partially rescue viability, demonstrating that neuronal death is driven by copper overload, not oxidative stress itself. These findings redefine the mechanistic framework linking copper redox imbalance to Aβ pathology and neuronal vulnerability and demonstrate a selective, sensitive approach for monitoring copper homeostasis and its disruption in neurodegenerative disease.

  PublisherOA PDFDOI

Recent grants

• NIH Grant R01ES016865

  NIH · $1.7M · 2014

• Biosynthetic Models of Heteronuclear Metalloenzymes in Multi-electron Processes

  NIH · $5.1M · 2001–2023

• Design and Selection of Novel Metalloenzymes for Biocatalysis, Bioimaging, and Genetic Engineering

  NIH · $2.8M · 2021–2026

• Novel DNAzyme sensors for lithium and sodium to understand cellular and molecular mechanisms of lithium treatment of bipolar disorder

  NIH · $401k · 2016–2019

• Modulation of Metalloprotein Activities through Fine-tuning Reduction Potentials

  NSF · $561k · 2021–2024

Frequent coauthors

• Edward I. Solomon

  SLAC National Accelerator Laboratory

  93 shared

• Juewen Liu

  University of Waterloo

  71 shared

• Britt Hedman

  Stanford Synchrotron Radiation Lightsource

  64 shared

• Keith O. Hodgson

  Stanford Synchrotron Radiation Lightsource

  64 shared

• Ninian J. Blackburn

  Oregon Health & Science University

  50 shared

• Hang Xing

  State Key Laboratory of Chemobiosensing and Chemometrics

  48 shared

• William B. Tolman

  Washington University in St. Louis

  46 shared

• Yang Yu

  Beijing Institute of Technology

  46 shared

Education

• PhD, Chemistry

  University of California at Los Angeles

  1992