About

Amy I-Lin Cheng is an Assistant Professor of Music at the University of Michigan School of Music, Theatre & Dance, where she serves as the Piano Chamber Music Coordinator. Born in Taiwan, she is an accomplished pianist with an extensive international performance career, having appeared on concert stages across the United States, Canada, Germany, Switzerland, Denmark, Taiwan, Brazil, France, and Israel. Her performances have been broadcast on various radio stations including WGBH, KCSC, WHYY, La Radio Suisse Romande-Espace 2, WFMT, and NPR. Cheng has performed recitals at notable venues such as the Isabella Stewart Gardner Museum, Merkin Concert Hall in New York City, Weill Recital Hall in Carnegie Hall, and the National Concert Hall in Taipei, and has appeared as a concerto soloist with numerous orchestras including the Musica Viva Moscow Chamber Orchestra, Taichung Philharmonic, and the University of Michigan Symphony Orchestra. She made her Boston concerto debut at age 17 under Benjamin Zander and has premiered works such as the Kaprálová Piano Concerto in North America, the Improvisation on Misirlou by Daniel Rein, and the Double Concerto for YangQin and Piano by Chun-Da Huang, collaborating with the National Chinese Orchestra Taiwan. Her recording of the Kaprálová concerto on Naxos received critical acclaim, and she has contributed to the publication of a new edition of the work. Cheng is also a dedicated chamber musician, co-Artistic Director of the Brightmusic Society of Oklahoma, and part of ensembles like Duo Clarion and Trio Solari, performing and recording extensively. She has collaborated with numerous distinguished artists and has been involved in many commissioning and premiering initiatives. An active educator, Cheng has given masterclasses internationally and mentors students who have achieved top prizes and scholarships. She holds degrees from the Curtis Institute of Music, Yale University School of Music, and the New England Conservatory, studying under renowned teachers such as Claude Frank and Wha-Kyung Byun. Prior to her current position, she served as Head of the Piano Area at Oklahoma City University and as Assistant Professor of Piano at Oklahoma State University. She joined the University of Michigan faculty in 2012 and has been a key figure in teaching studio piano and chamber music.

Research topics

• Endocrinology
• Medicine
• Food science
• Mathematical analysis
• Chemistry
• Mathematics
• Internal medicine

Selected publications

• Quantifying glucose uptake at the single cell level with confocal microscopy reveals significant variability within and across individuals

  Scientific Reports · 2025-01-21 · 2 citations

  articleOpen access

  Measurement of glycated hemoglobin (HbA1c) in human red blood cells plays a critical role in the diagnosis and treatment of diabetes mellitus. However, recent studies have suggested large variation in the relationship between average glucose levels and HbA1c, creating the need to understand glucose variability at the cellular level. Here, we devised a fluorescence-based method to quantitatively observe GLUT1-mediated intracellular glucose analog tracer uptake in individual RBCs utilizing microfluidics and confocal microscopy. For the first time, we demonstrate that intracellular/extracellular tracer percentages can be measured at the single cell level using the fluorescently labeled glucose analog, 2-NBDG. A small donor panel study indicates that the characteristic intracellular 2-NBDG percentages can statistically differ based on race (i.e., Caucasian/Hispanic vs Black). RBC intracellular glucose analog tracer 2-NBDG levels show significant variability both from cell-to-cell and from donor-to-donor. This specific transport mechanism will affect HbA1c formation in erythrocytes. This finding further supports a more personalized, and perhaps improved, diagnostic strategy for diabetes.

  PublisherOA PDFDOI

• Fyn-T Kinase Regulates DHA-Induced Pyroptosis in Immortalized Normal Human Astrocytes

  Preprints.org · 2025-09-22

  preprintOpen access1st authorCorresponding

  Dysregulation of astroglia-mediated neuroinflammation is known to be involved in neurodegen-erative diseases. Amongst multiple inflammatory pathways, pyroptosis is characterized by in-flammatory cell death following inflammasome activation. Recently, the omega-3 poly-unsaturated fatty acid, DHA, has been identified as a pyroptosis inducer, although the un-derlying mechanisms remain unclear. In this study, we investigated the role of the alternative-ly-spliced T-isoform of Fyn kinase (FynT) in DHA-induced astroglial pyroptosis. Immortalized normal human astrocytes (iNHA) expressing wild-type FynT (FynT-WT), kinase-dead mutant FynT (FynT-KD), or empty vector (EV) controls were treated with DHA and assessed for pyrop-totic activation. We found that DHA-treated FynT-WT cells exhibited significantly reduced cyto-solic lactate dehydrogenase release, pyroptotic morphology and markers (cleaved caspase-1 and its substrates, cleaved caspase-3 and gasdermin-D N fragments) compared to either EV or FynT-KD cells. No significant differences in pyroptotic activation were observed between EV and FynT-KD cells. In addition, no differences in immunoreactivities of pro- or anti-apoptotic markers (Bax or Bcl-2) were observed across the DHA-treated cells. In summary, our study postulates a negative regulatory role of FynT kinase on DHA-induced pyroptosis in astrocytes, with implica-tions for further understanding neuroinflammatory mechanisms in neurodegenerative diseases and identification of potential therapeutic targets.

  PublisherOA PDFDOI

• Fyn-T Kinase Regulates DHA-Induced Pyroptosis in Immortalized Normal Human Astrocytes

  Cells · 2025-09-30

  articleOpen access1st author

  Dysregulation of astroglia-mediated neuroinflammation is known to be involved in neurodegenerative diseases. Amongst multiple inflammatory pathways, pyroptosis is characterized by inflammatory cell death following inflammasome activation. Recently, the omega-3 poly-unsaturated fatty acid, DHA, has been identified as a pyroptosis inducer, although the underlying mechanisms remain unclear. In this study, we investigated the role of the alternatively spliced T-isoform of Fyn kinase (FynT) in DHA-induced astroglial pyroptosis. Immortalized normal human astrocytes (iNHA) expressing wild-type FynT (FynT-WT), kinase-dead mutant FynT (FynT-KD), or empty vector (EV) controls were treated with DHA and assessed for pyroptotic activation. We found that DHA-treated FynT-WT cells exhibited significantly reduced cytosolic lactate dehydrogenase release, pyroptotic morphology and markers (cleaved caspase-1 and its substrates, cleaved caspase-3 and gasdermin-D N fragments) compared to either EV or FynT-KD cells. No significant differences in pyroptotic activation were observed between EV and FynT-KD cells. In addition, no differences in immunoreactivities of pro- or anti-apoptotic markers (Bax or Bcl-2) were observed across the DHA-treated cells. In summary, our study postulates a negative regulatory role of FynT kinase in DHA-induced pyroptosis in astrocytes, with implications for further understanding neuroinflammatory mechanisms in neurodegenerative diseases and identification of potential therapeutic targets.

  PublisherOA PDFDOI

• Association of HbA1c and an updated glucose management indicator (uGMI) with incident diabetic retinopathy in adults with type 1 diabetes: a longitudinal study

  Diabetologia · 2025-11-11 · 2 citations

  articleOpen access

  Abstract Aims/hypothesis This study aimed to compare the predictive performance of HbA 1c and a continuous glucose monitoring (CGM)-based updated glucose management indicator (uGMI) in assessing incident diabetic retinopathy risk. Methods We used the data from a previously published longitudinal case–control study that collected CGM data for up to 7 years prior to diagnosis of incident diabetic retinopathy or no retinopathy (control participants) among adults with type 1 diabetes. Mutual information scores (MIS), receiver operating characteristics (ROC) curves and machine learning models were used to assess the associations of diabetic retinopathy with HbA 1c , uGMI and CGM-derived metrics. Results The uGMI demonstrated a stronger association with incident diabetic retinopathy (MIS 0.148) compared with HbA 1c (MIS 0.078). ROC analysis showed that uGMI had a modestly higher AUC (AUC 0.733) than HbA 1c (AUC 0.704). Decision tree models incorporating both HbA 1c and uGMI did not improve clinically significant diabetic retinopathy risk prediction. Machine learning models confirmed the better predictive value of uGMI, especially for HbA 1c values between 54 mmol/mol (7.1% NGSP) and 58 mmol/mol (7.5% NGSP), where diabetic retinopathy risk escalated significantly. Conclusions/interpretation The uGMI is a slightly stronger predictor of diabetic retinopathy risk compared with HbA 1c . HbA 1c and uGMI do not appear to be complementary for diabetic retinopathy risk prediction. Graphical Abstract

  PublisherOA PDFDOI

• Variation in the relationship between fasting glucose and HbA1c: implications for the diagnosis of diabetes in different age and ethnic groups

  BMJ Open Diabetes Research & Care · 2024-03-01 · 9 citations

  articleOpen access

  INTRODUCTION: Identify non-glycemic factors affecting the relationship between fasting plasma glucose (FPG) and glycated hemoglobin (HbA1c), in order to refine diabetes diagnostic criteria. RESEARCH DESIGN AND METHODS: Relationship between FPG-HbA1c was assessed in 12 531 individuals from 2001 to 2018 US National Health and Nutrition Examination Survey. Using a recently described method, FPG and HbA1c were used to calculate apparent glycation ratio (AGR) of red blood cells for different subgroups based on age, race, and gender. RESULTS: At an FPG of 7 mmol/L, black individuals had a higher HbA1c (p<0.001, mean: 50.2 mmol/mol, 95% CI (49.8 to 50.4)) compared with white individuals (47.4 mmol/mol (47.2 to 47.5)). This corresponds to NGSP (National Glycohemoglobin Standardization Program) units of 6.7% and 6.5% for black versus white individuals, respectively. Similarly, individuals under 21 years had lower HbA1c (p<0.001, 47.9 mmol/mol (47.7 to 48.1), 6.5%) compared with those over 50 years (48.3 mmol/mol (48.2 to 48.5), 6.6%). Differences were also observed between women (p<0.001, 49.2 mmol/mol (49.1 to 49.3), 6.7%) and men (47.0 mmol/mol (46.8 to 47.1), 6.5%). Of note, the difference in HbA1c at FPG of 7 mmol/L in black females over 50 and white males under 21 years was 5 mmol/mol (0.46%). AGR differences according to race (p<0.001), age (p<0.001), and gender (p<0.001) explained altered glucose-HbA1c relationship in the analyzed groups. CONCLUSIONS: FPG-HbA1c relationship is affected by non-glycemic factors leading to incorrect diagnosis of diabetes in some individuals and ethnic groups. Assessment of AGR helps understand individual-specific relationship between glucose levels and HbA1c, which has the potential to more accurately diagnose and manage diabetes.

  PublisherOA PDFDOI

• Time in Range, Time in Tight Range, and Average Glucose Relationships Are Modulated by Glycemic Variability: Identification of a Glucose Distribution Model Connecting Glycemic Parameters Using Real-World Data

  Diabetes Technology & Therapeutics · 2024 · 14 citations

  • Medicine
  • Internal medicine
  • Endocrinology

  The gamma model accurately predicts interactions between CGM-derived glycemic metrics and reveals that glycemic variability can significantly influence the relationship between AG and TIR with opposing effects according to AG levels. Our findings potentially help with clinical diabetes management, particularly when AG and TIR appear mismatched.

  PublisherDOI

• Evaluation of continuous glucose monitoring‐derived person‐specific <scp>HbA1c</scp> in the presence and absence of complications in type 1 diabetes

  Diabetes Obesity and Metabolism · 2022 · 7 citations

  • Food science
  • Medicine
  • Chemistry

  AIM: To evaluate the accuracy of a novel kinetic model at predicting HbA1c in a real-world setting and to understand and explore the role of diabetes complications in altering the glucose-HbA1c relationship and the mechanisms involved. MATERIALS AND METHODS: Deidentified HbA1c and continuous glucose monitoring values were collected from 93 individuals with type 1 diabetes. Person-specific kinetic variables were used, including red blood cell (RBC) glucose uptake and lifespan, to characterize the relationship between glucose levels and HbA1c. The resulting calculated HbA1c (cHbA1c) was compared with glucose management indicator (GMI) for prospective agreement with laboratory HbA1c. RESULTS: = 0.85 and 0.44, respectively. The fraction within 10% of absolute relative deviation from laboratory HbA1c was 93% for cHbA1c and 63% for GMI. Macrovascular disease had no effect on the model's accuracy, whereas microvascular complications resulted in a trend towards higher HbA1c, secondary to increased RBC glucose uptake. CONCLUSIONS: cHbA1c, which takes into account RBC glucose uptake and lifespan, accurately reflects laboratory HbA1c in a real-world setting and can aid in the management of individuals with diabetes.

  PublisherOA PDFDOI

• Biological Functions for STARD5 Assessed Using <i>stard5</i> ^{<i>−/−</i>} Mice

  The FASEB Journal · 2020-04-01 · 1 citations

  articleSenior author

  STARD5 belongs to the StAR‐Related Lipid‐transfer (START) domain protein superfamily and is proposed to contribute to intracellular non‐vesicular cholesterol transport. STARD5 is a soluble sterol‐binding protein that is induced by endoplasmic reticulum (ER) stress, yet testing for a biological function needs to consider the conflicting data on whether the preferred ligand for STARD5 is cholesterol and 25‐hydroxycholesterol or bile acids, including chenodeoxycholic acid (CDCA). Our work has characterized STARD5 expression in kidney and we reported that STARD5 and cholesterol levels are increased in kidneys of the OVE diabetic mouse model compare to wild‐type controls, and that STARD5 is increased in cell culture by the ER stress inducer tunicamycin. Cholesterol accumulation in the ER is known to promote ER stress; however, the significance of the association between elevated renal cholesterol, ER stress, and STARD5 in diabetic kidney remains to be determined. We propose STARD5 indirectly controls cholesterol homeostasis via modulating farnesoid X receptor (FXR) activity. FXR is a nuclear receptor that binds CDCA and activation of FXR contributes to maintaining fatty acid and cholesterol homeostasis in diabetic kidney disease. To test whether STARD5 affects FXR signaling we generated whole body STARD5 knock‐out mice ( stard5 −/− ) using CRISPR‐Cas9 and compared the FXR target gene expression in the knockout and WT kidney. There was no difference in body weight, liver weight/body weight ratio, or kidney weight/body weight ratio between stard5 −/− mice compared to wild‐type littermate controls (WT) (male mice n = 5 WT; n= 7 stard5 −/− ) . We will present data from current studies focused on determining whether there are differences in tissue histology, lipid accumulation, and FXR target gene expression between stard5 −/− mice and WT littermate controls. Support or Funding Information Biochemistry &amp; Molecular Genetics Departmental Funds to BJC

  PublisherDOI

• Licensing increases the quantity and immunomodulatory cargo of mesenchymal stromal cell exosomes

  Cytotherapy · 2018-04-27

  article1st authorCorresponding
  PublisherDOI

• Mechanosensitive ion channels in articular nociceptors drive mechanical allodynia in osteoarthritis

  Journal of Pain · 2018-02-13

  article
  PublisherDOI

Recent grants

• NIH Grant R56DK093847

  NIH · $375k · 2014

Frequent coauthors

• Michel L. Tremblay

  38 shared

• Noriko Uetani

  27 shared

• Mounib Elchebly

  Jewish General Hospital

  27 shared

• Luce Dombrowski

  Université Laval

  25 shared

• Robert A. Mooney

  Johns Hopkins University

  25 shared

• Mélanie J. Chagnon

  McGill University

  25 shared

• André Marette

  Montreal Heart Institute

  25 shared

• Wen H. Yu

  Wuhan University of Technology

  21 shared

Education

• Ph.D., Biochemistry

  McGill University

  2003

• MSc., Biochemistry

  University of Ottawa

  1996

• BSc., Biochemistry

  University of Ottawa

  1995