About

Ming-Lin Liu, MBBS, PhD, is a Research Associate Professor of Dermatology at the University of Pennsylvania's Perelman School of Medicine. His research expertise focuses on the function of Extracellular Vesicles (EVs) and Neutrophil Extracellular Traps (NETs) as critical mediators of cell-to-cell communication and inflammation in health and disease. He conducts mechanistic studies on programmed cell death, such as NETosis, and the regulation of EV generation and NET formation, exploring their roles in innate immunity and autoimmunity. His work includes investigating the pathogenesis of autoimmune diseases, including systemic lupus erythematosus (SLE), Dermatomyositis, and Vasculitis, particularly how EVs and NETs are mediated and modulated by factors like UV light and tobacco smoking. Additionally, Liu studies the role of EVs in cardiometabolic and vascular pathology, examining how tobacco smoking influences EV release and function to drive disease progression. His contributions aim to deepen understanding of immune mechanisms and inflammatory processes, with implications for autoimmune and vascular diseases.

Research topics

• Cell biology
• Biology
• Medicine
• Internal medicine
• Chemistry

Selected publications

• Machine learning-based identification of biochemical markers to predict hepatic steatosis in patients at high metabolic risk

  World Journal of Gastroenterology · 2025-07-18 · 2 citations

  articleOpen access

  BACKGROUND: Metabolic-associated fatty liver disease (MAFLD) is the most common cause of chronic liver disease and remains under-recognized within the health check-up population. Ultrasonography during physical examination fail to accurately identify at-risk patients as they involve multiple metabolic aspects. AIM: To rapidly identify hepatic steatosis patients from high-metabolic-risk populations and reduce medical costs. METHODS: We analyzed all data from a prospective cohort study to identify potential predictors of MAFLD risk. The LASSO and recursive feature elimination were used to screen for feature selection. Four machine learning models were employed to construct the prediction model for hepatic steatosis. RESULTS: 504 MAFLD patients) were included, and the prediction models were validated. After overlapping and reducing the feature set based on feature importance ranking, we developed an interpretable final XGBoost model with 10 features, achieving an area under the curve of 0.82. CONCLUSION: We have introduced a valuable noninvasive tool for efficiently identifying hepatic steatosis patients in high-metabolic-risk populations. This tool may improve screening effectiveness and reduce medical costs.

  PublisherDOI

• A Glucose-Responsive Donor–Acceptor Polymer with Dual Aie–Pet Fluorescence Switching: Synthesis, Structural Characterization, and Selective Sensing Performance

  SSRN Electronic Journal · 2025-01-01

  preprintOpen access
  PublisherDOI

• Ashes to Rashes: An Exploration of the Intersection Between Smoking and Cutaneous Lupus Erythematosus

  Biomolecules · 2025-08-29

  reviewOpen access

  Cutaneous lupus erythematosus is an autoimmune skin disorder with a known association with cigarette smoking. Smokers with cutaneous lupus have a worse disease course and may be refractory to treatments. Despite many studies documenting this association, minimal work exists examining the molecular drivers of these clinical differences. This review delves into how cigarette smoke may influence key immunopathogenic pathways in cutaneous lupus, including oxidative stress, interferon signaling, inflammatory cell recruitment, extracellular vesicles, and immune regulation. Additionally, factors such as epigenetics and heat injury are considered as well. Here, we integrate the existing and emerging literature on the pathophysiology of cutaneous lupus with known effects of cigarette smoke on the skin and immune system and propose hypotheses that may explain clinical differences in smokers. Understanding the molecular underpinnings of these differences may yield a clearer picture of the disease and more effective treatment strategies.

  PublisherOA PDFDOI

• Preparation of graphite felt-supported Pt monolithic catalyst for low-temperature oxidation of benzene in an electric field

  SSRN Electronic Journal · 2025-01-01

  preprintOpen access1st authorCorresponding
  PublisherDOI

• From acute tubular injury to tubular repair and chronic kidney diseases – KIM-1 as a promising biomarker for predicting renal tubular pathology

  Current Research in Physiology · 2025-01-01 · 12 citations

  reviewOpen accessSenior authorCorresponding

  Kidney Injury Molecule-1 (KIM-1) has emerged as a significant biomarker and mechanistic player in kidney pathology, particularly in acute kidney injury (AKI). Normally absent in healthy kidney proximal tubules, KIM-1 becomes upregulated specifically along the proximal tubule cells' surface in response to acute injury, reflecting the differential vulnerability of convoluted versus straight proximal tubules. Functionally, KIM-1 aids proximal tubules in clearing apoptotic cells and moderating inflammatory responses, thereby helping to prevent excessive immune activation during the early stages of injury. Clinically, KIM-1 is a sensitive, non-invasive biomarker for detecting proximal tubular injury, allowing for assessment in urine, plasma samples, and tissue biopsies in AKI. However, if tubular injury persists without repair, prolonged KIM-1 expression can drive chronic inflammatory responses and interstitial fibrosis, leading to chronic kidney disease (CKD). In addition, KIM-1's role may extend further into promoting tubular dedifferentiation, potentially contributing to renal cell carcinoma under certain conditions. Over the past two decades, KIM-1 research has reshaped our understanding of kidney pathophysiology and immunology, spanning acute injury responses to chronic disease progression. This review aims to provide an updated synthesis of recent findings, highlighting KIM-1's role across the spectrum of renal injury and repair.

  PublisherDOI

• Characterizing Keratinocyte-Derived Extracellular Vesicles in UVB-Irradiated Murine Skin

  JID Innovations · 2025-08-22

  articleOpen access

  UVB radiation is a potent trigger for photosensitive autoimmune diseases, yet the mechanism through which UVB-induced superficial epidermal damage drives deeper systemic inflammation remains poorly understood. Extracellular vesicles (EVs) have emerged as key mediators of UVB-induced immune activation and have also been specifically implicated in the pathogenesis of multiple photosensitive autoimmune diseases, therefore suggesting the possibility that UVB-induced EVs could be involved in driving this systemic inflammation. In this study, C57BL/6 mice were exposed to repeated dorsal UVB irradiation, and dermal tissue was processed to isolate EVs through sequential ultracentrifugation and density-gradient purification. Transmission electron microscopy, ExoView, immunogold labeling, and western blotting confirmed the presence of EVs within the dermis, including those expressing cytokeratin 10, a keratinocyte differentiation marker. UVB-irradiated dermal EVs showed significantly higher cytokeratin 10 expression than sham controls, supporting their keratinocyte origin and demonstrating that EVs can traverse the epidermal-dermal junction. These findings provide direct evidence that UVB triggers the release of keratinocyte-derived EVs into the dermis, where they may serve as vehicles for inflammatory signaling and immune modulation. The identification of cytokeratin 10-positive EVs as mediators of epidermal-dermal crosstalk highlights a potential mechanism linking UVB exposure to systemic autoimmunity and suggests, to our knowledge, a previously unreported therapeutic targets to mitigate photodamage.

  PublisherOA PDFDOI

• Macrocycle-Based Zn-Mofs with Switchable Zn²⁺-Acylhydrazone Coordination for Enzyme-Mimetic Adaptive Lewis Acid Catalysis

  SSRN Electronic Journal · 2025-01-01

  preprintOpen access
  PublisherDOI

• Electroacupuncture Ameliorates Airway Dysbiosis and Inflammation by Modulating Circadian Rhythm in COPD Mice

  American Journal of Respiratory and Critical Care Medicine · 2025-05-01

  article

  Abstract Rationale: Airway dysbiosis has been shown to enhance pulmonary inflammation in COPD. However, the upstream mechanisms that modulate airway microbiota remain largely unexplored. Circadian disruption, also a feature of COPD, can alter microbiome communities and inflammatory pathways in the gut. However, whether circadian disruption contributes to airway dysbiosis in COPD is unknown. Electroacupuncture is an effective way of modulating circadian rhythm and shows beneficial effect in COPD. Yet whether electroacupuncture can ameliorate airway dysbiosis by modulating circadian rhythm is unclear. Methods: We utilized male C57BL/6J and BMAL1 knockout mice, subjected to intranasal challenges with elastase (ELT) and lipopolysaccharide (LPS) over four weeks to establish a COPD model. Electroacupuncture treatment at Zeitgeber time (ZT0) or ZT12 was applied to bilateral Zusanli acupoints (ST36) for 15 minutes per day over two weeks. All specimens were collected at ZT0 for analysis. Lung tissues were examined through H&E staining, 16S rRNA sequencing, and quantification of key circadian rhythm molecules using qPCR and Western blotting, while bronchoalveolar lavage (BAL) was performed for inflammatory cell counts. Results: The COPD model was confirmed by significant airflow limitation (FEV200/FVC), increased airway resistance, reduced airway compliance, and notable inflammatory cell infiltration in lung tissues. COPD mice exhibited significant airway microbial dysbiosis characterized by reduced biodiversity that was reflected by lower Shannon, Evenness, and Sobs indices. Concomitantly, circadian clock functioning was also disturbed in the context of COPD, as evidenced by downregulation of key clock molecules (BMAL1, CLOCK, NR1D1, CRY1, PER1, and PER2) at both genetic and protein levels. BMAL1 knockout amplified airway inflammation in COPD mice and more noticeably, exacerbated airway dysbiosis (lower diversity indices). Interestingly, electroacupuncture at ZT12 rather than ZT0 markedly upregulated the expression of the above circadian clock-related molecules in COPD mice and also ameliorated airway dysbiosis (increased diversity indices) and inflammation. Conclusion: Circadian disruption exacerbates airway dysbiosis and inflammation in COPD mice. Electroacupuncture at ST36 ameliorates airway dysbiosis and inflammation by modulating circadian rhythm. This study provides evidence on host's circadian control of airway microbiota and new insights into how we can practically modulate circadian clock and microbiota for the treatment of respiratory diseases.

  PublisherDOI

• Extracellular Vesicles in the Pathogenesis, Clinical Characterization, and Management of Dermatomyositis: A Narrative Review

  International Journal of Molecular Sciences · 2024-02-06 · 8 citations

  reviewOpen access

  Extracellular vesicles (EVs) are lipid-bilayer particles secreted from cells that primarily assist in cell-to-cell communication through the content of their cargo, such as proteins and RNA. EVs have been implicated in the pathogenesis of various autoimmune diseases, including dermatomyositis (DM), an inflammatory autoimmune disease characterized by distinct cutaneous manifestations, myopathy, and lung disease. We sought to review the role of EVs in DM and understand how they contribute to the pathogenesis and clinical characterization of the disease. We summarized the research progress on EVs in dermatomyositis based on recent publications. EV cargoes, such as double-stranded DNA, microRNA, and proteins, contribute to DM pathogenesis and mediate the proinflammatory response and cytokine release through signaling pathways such as the stimulator of interferon genes (STING) pathway. These nucleic acids and proteins have been proposed as disease-specific, stable biomarkers to monitor disease activity and responses to therapy. They also correlate with clinical parameters, inflammatory markers, and disease severity scores. Furthermore, some markers show an association with morbidities of DM, such as muscle weakness and interstitial lung disease. The continued study of EVs will help us to further elucidate our understanding of dermatomyositis.

  PublisherOA PDFDOI

• Keratinocyte derived extracellular vesicles mediated crosstalk between epidermis and dermis in UVB-induced skin inflammation

  Cell Communication and Signaling · 2024-09-30 · 15 citations

  articleOpen access

  BACKGROUND AND RATIONALE: Ultraviolet-B (UVB) light induces dermal inflammation, although it is mostly absorbed in the epidermis. Recent reports suggest extracellular vesicles (EVs) act as a mediator of photodamage signaling. Melatonin is reported to be a protective factor against UV-induced damage. We hypothesized that EVs derived from UVB-irradiated keratinocytes might trigger proinflammatory responses in dermal cells and tested whether melatonin can ameliorate UVB-induced inflammation. METHODS: We used UVB-irradiated HaCaT cells, primary keratinocytes and STING knock-out mice to model production of EVs under photodamaging conditions and performed immunoblotting and ELISA to measure their effect on dermal macrophages. RESULTS: UVB-irradiated keratinocytes produce an increased number of EVs that contain higher concentrations of DNA and protein compared with controls. KC-derived EVs (KEVs) induced a STING- and inflammasome-mediated proinflammatory response in macrophages in vitro, and a pronounced inflammatory infiltrate in mouse dermis in vivo. Melatonin ameliorated KEVs inflammatory effect both in vitro and in vivo. CONCLUSIONS: This data suggests EVs are mediators in a crosstalk that takes place between keratinocytes and their neighboring cells as a result of photodamage. Further studies exploring EVs induced by damaging doses of UVB, and their impact on other cells will provide insight into photodamage and may help develop targeted therapeutic approaches.

  PublisherOA PDFDOI

Recent grants

• Extracellular vesicle-associated MAVS and IFNẞ in Dermatomyositis

  NIH · $443k · 2019–2022

Frequent coauthors

• Victoria P. Werth

  Philadelphia VA Medical Center

  45 shared

• Kevin Jon Williams

  34 shared

• Moritz Mall

  Central Institute of Mental Health

  22 shared

• Marja‐Riitta Taskinen

  22 shared

• Xing Lyu

  18 shared

• Kati Ylitalo

  18 shared

• Yae Jin Yoon

  16 shared

• Diana Noronha Nunes

  AC Camargo Hospital

  16 shared

Labs

• Ming-Lin Liu LaboratoryPI

Education

• MBBS

  Tianjin Medical University

  1986