About

Jane P. Kim is a Clinical Assistant Professor in the Department of Psychiatry and Behavioral Sciences at Stanford University. She is affiliated with the Center for Artificial Intelligence in Medicine & Imaging (AIMI) at Stanford. Her work focuses on the application of artificial intelligence in medicine and imaging, contributing to research and education in these areas. As part of her role, she is involved in advancing AI-driven healthcare solutions and fostering collaboration between academia and industry to improve medical imaging and psychiatric care.

Research topics

• Internal medicine
• Medicine
• Organic chemistry
• Biology
• Biochemistry
• Cell biology
• Anatomy
• Chemistry
• Environmental health

Selected publications

• Pilot proteomics study for identifying a pollution exposure signature in firefighters

  Journal of Exposure Science & Environmental Epidemiology · 2026-04-13

  articleOpen access

  BACKGROUND: Recent studies showed that immune and cardiometabolic biomarker levels increased in individuals exposed to air pollution. OBJECTIVE: We sought to identify a pollution exposure signature in a pilot cohort of 54 firefighters and controls in the Bay Area. METHODS: We analyzed Olink-processed proteomics data under multiple approaches for feature selection, including the LASSO. We selected 67 biomarkers related to well-defined pathways for targeted analyses, whereas 1463 unique assays were considered for untargeted analyses. RESULTS: Levels of angiopoietin 1 and hydroxyacylglutathione hydrolase were consistently higher in firefighters compared to controls. Moreover, matrix metalloproteinase-1, a protein that promotes tumorigenesis, was higher at the visit with greater acute exposure. Fifteen other key biomarkers were jointly identified under untargeted and targeted approaches. Regression analysis found that 10 biomarkers were numerically higher in firefighters with high exposure. SIGNIFICANCE: These analyses demonstrate the potential utility of large-scale plasma proteomics in identifying a pollution exposure signature. IMPACT STATEMENT: Exposure to particulate matter leads to proteomic changes that are associated with adverse health outcomes. Applying regularization-based feature selection methods to high-dimensional data can identify a small subset of biomarkers for targeted monitoring efforts. Our findings improve understanding of the implications of air pollution for healthy adults and serve as a foundation to developing strategies for mitigating occupational exposure.

  PublisherDOI

• Workplace Pollution and Risk of Incident Coronary Artery Disease

  medRxiv · 2026-01-19

  articleOpen access

  Importance: Genetic factors only explain ~50% of an individual's lifetime CAD risk. Workplace pollution exposure likely represents a significant, under-recognized, and modifiable contributor. Clarifying its independent effect - distinct from residential air pollution - could inform targeted prevention, clinical risk assessment, and policy strategies. Objective: To quantify the independent association between workplace pollution exposure and incident CAD, rigorously adjusting for canonical risk factors, genetic risk, socioeconomic deprivation index, and residential air pollution. Design Setting and Participants: A prospective cohort analysis of 103,599 adults in the UK Biobank with complete baseline employment history and specialized workplace environment surveys. Participants with prior CAD, or missing genetic information, canonical risk factor data, or residential air pollution measurements, were excluded. Exposure: Cumulative, self-reported duration of exposure to workplace pollutants (including dust, smoke, exhaust, chemicals, asbestos, paints, and pesticides), summarized as a percentile measure. Main Outcomes and Measures: Incident CAD. Associations were estimated using Cox proportional hazards models adjusted for demographics, comorbidities, CAD polygenic risk score, and residential air pollution metrics, accounting for competing death events. Results: The cohort (median age 64 years; 43% male) had high baseline prevalence of smoking (41%) and co-morbidities (hypertension 27%, hyperlipidemia 16%, diabetes 4.3%). Common exposures included smoke (56%), dust (39%), and chemicals (27%). Over a median 7.5-year follow-up, 4,327 CAD cases occurred. Compared to the low exposure group, high workplace pollution exposures showed a stronger unadjusted association with CAD (hazard ratio [HR], 1.51; 95% CI, 1.40-1.63) relative to residential air pollution (unadjusted HR, 1.23; 95% CI, 1.14-1.33). Importantly, in multivariable models, workplace pollution remained independently associated with higher CAD incidence (adjusted HR, 1.21; 95% CI, 1.03-1.41), robust to all adjustment. Significant specific drivers included paints, thinners or glues, diesel exhaust, fumes, asbestos, and dust. Conclusions and Relevance: Workplace pollution is confirmed as a robust, independent risk factor for incident CAD. Its association is demonstrably stronger than residential air pollution and persists despite comprehensive adjustment for genetic predisposition and traditional cardiovascular risk factors. These findings underscore the need to strengthen worker protections, integrate occupational history into clinical risk assessment, and prioritize mechanistic research into non-lipid pollution pathways.

  PublisherOA PDFDOI

• Abstract Tu0087: Uncovering Sex-Specific Mechanisms in Vascular Disease through a Multi-Omics Approach

  JVS Vascular Science · 2026-01-01

  articleOpen access
  PublisherDOI

• Reframing Cardiovascular Interventions in Cancer Patients: Emerging Evidence and Evolving Paradigms

  Current Treatment Options in Cardiovascular Medicine · 2026-01-03

  articleSenior authorCorresponding
  PublisherDOI

• Polyethylene and Polyvinyl Chloride Nanoplastics Accelerate Atherosclerosis Through Distinct Smooth Muscle Cell Phenotypes

  medRxiv · 2026-02-14

  articleOpen accessSenior authorCorresponding

  Abstract Micro- and nanoplastics (MNPs) are increasingly detected in human tissues, yet their causal contribution to cardiovascular disease remains poorly understood. Here we show that oral exposure to polyethylene (PE) and polyvinyl chloride (PVC) -- the most abundant polymers found in human atheromas -- accelerates atherosclerosis in ApoE-/-mice through distinct, polymer-specific molecular mechanisms. While both polymers increased plaque burden and reduced contractile smooth muscle cell (SMC) markers, single-cell transcriptomic profiling revealed divergent phenotypic trajectories. PE exposure drives SMCs toward a chondromyocyte-like cell (CMC) state, characterized by upregulated osteogenic signaling and markedly increased vascular calcification. Conversely, PVC exposure promotes a fibromyocyte-like program associated with altered collagen metabolism and accelerated cell migration without enhancing calcification. These distinct SMC programs are reflected in the transcriptional signatures of symptomatic human carotid plaques, suggesting clinical relevance for polymer-specific vascular remodeling. Our findings establish a causal link between common environmental plastics and accelerated atherosclerosis, demonstrating that MNP-induced vascular risk is mediated by divergent SMC fate decisions. These results provide a mechanistic framework for assessing the cardiovascular impact of global plastic pollution and identifying potential therapeutic targets to mitigate MNP-associated vascular toxicity.

  PublisherOA PDFDOI

• Abstract Tu0087: Uncovering Sex-Specific Mechanisms in Vascular Disease through a Multi-Omics Approach

  Arteriosclerosis Thrombosis and Vascular Biology · 2025-04-01

  article

  Background: Vascular diseases are a leading cause of mortality worldwide. Epidemiological data suggest significant sex-based differences in vascular disease risk, but the mechanisms underlying these differences remain unclear. Clinical observations indicate that key sex-specific differences may exist in the vessel wall. Hypothesis: We hypothesize that sex differences in vascular diseases are regulated by sex-specific epigenetic factors/features that alter cellular responses to pathologic triggers in the vessel wall. Methods: Single cell transcriptomic (scRNA-seq) and epigenetic (scATAC-seq) analyses were performed on male (M) and female (F) ApoE mice at different stages of atherosclerosis progression (0, 16 wks) to uncover sex-specific responses to vascular insult. Comparative analyses were performed on M and F human coronary arteries to identify biologically conserved sex-specific regulatory features shared between humans and mice. These features were integrated with human genetic data to identify the biological processes and regulatory regions driving sex-specific responses. Key findings were subsequently validated in vitro using primary human vascular cells. Results: Transcriptomic differences between M and F cells were most profound in smooth muscle cells (SMC) and fibroblasts in human and murine arteries. In mouse, the sex-specific transcriptomic differences drastically increased after high fat diet exposures, with number of differentially expressed genes increasing from 29 to 140 in SMC, and 63 to 181 in fibroblasts. Furthermore, we found F SMC to more readily undergo phenotypic modulation despite lower lipid levels. Gene set enrichment analysis showed increased pathways related to extracellular matrix organization and epigenetic modification, as well as key regulators of PDGF and TGFB signaling in mice and human female SMC. Additionally, scATAC-seq identified thousands of sex-specific differentially accessible regions enriching for human genetic signals of vascular diseases. In particular, X-escapee genes Kdm6a and Kdm5c were identified which may work in concert to alter the epigenetic landscape. Conclusion: This study reveals significant sex-specific, vascular cell-type specific transcriptional and epigenetic mechanisms in vascular disease. These findings provide insights into the genetic and molecular basis of sex differences in vascular diseases and potential therapeutic targets.

  PublisherDOI

• Enhancer-targeting CRISPR screens at coronary artery disease loci suggest shared mechanisms of disease risk

  medRxiv · 2025-09-02 · 3 citations

  preprintOpen access

  To systematically identify causal genetic mechanisms that confer risk for coronary artery disease (CAD) in GWAS loci, we mapped genome-wide variant-to-enhancer-to-gene (V2E2G) links in vascular smooth muscle cells (SMC). Enhancers identified by active chromatin features, and further prioritized by base-resolution deep learning models of chromatin accessibility in 108 CAD loci, were studied with CRISPRi targeting and Direct-Capture Targeted Perturb-seq (DC-TAP-seq) evaluation of 470 genes. Seventy-six V2E2G links were identified for 59 candidate CAD genes representing gene programs including epithelial-mesenchymal transformation, ubiquitination, and protein folding as well as BMP and TGFB signaling. Similar methods employed with an independent focused screen targeting one candidate locus at 9p21.3 identified 10 enhancers regulating expression of multiple genes at this location. Detailed molecular studies revealed that two enhancers mediating transcription factor binding and transcriptional regulation contribute to ancestry-specific and sex-specific risk for CAD and the surrogate biomarker vascular calcification. Together, these studies advance our identification of GWAS CAD V2E2G links across the genome, and specific mechanisms of risk at the complex 9p21.3 locus.

  PublisherOA PDFDOI

• Environmental pollutants and atherosclerosis: Epigenetic mechanisms linking genetic risk and disease

  Atherosclerosis · 2025-02-15 · 14 citations

  reviewOpen accessSenior author
  PublisherOA PDFDOI

• Pilot proteomics study suggests elevated tumorigenesis-promoting biomarkers in healthy adults after air pollution exposure

  medRxiv · 2025-09-14

  preprintOpen access

  Abstract Objectives Recent studies have shown that immune and cardiometabolic biomarker levels increased in individuals exposed to ambient air pollution. We sought to explore the feasibility of identifying a pollution exposure signature using the Olink Explore platform in a small, pilot cohort of firefighters and age-matched controls in the Bay Area. Methods Demographics and plasma samples were collected at two study visits, one following the resolution of California’s record-setting 2020 wildfires and another in the spring of 2021. Age-matched samples were processed on the same plate, with 10 repeated on a second plate for assessing inter-plate variation. For comparing firefighter profile with healthy controls, we analyzed Olink proteomics data under multiple approaches for feature selection, including LASSO (the least absolute shrinkage and selection operator), elastic net, and PLS-DA (partial least squares discriminant analysis). In addition, we selected 67 biomarkers related to well-defined pathways for targeted analyses, whereas 1463 unique assays were considered for untargeted analyses. Results Our analysis found that levels of angiopoietin 1 and hydroxyacylglutathione hydrolase were consistently higher in firefighters compared to controls. Moreover, matrix metalloproteinase-1, a protein that promotes tumorigenesis, was higher at the visit with greater acute exposure. Fifteen other key biomarkers were jointly identified under untargeted and targeted approaches. When comparing targeted biomarkers in firefighters by level of exposure using a mixed effects regression model, 10 were found to be numerically higher in firefighters with high exposure. Conclusions These analyses demonstrate the potential utility of large-scale plasma proteomics in identifying a pollution exposure signature.

  PublisherOA PDFDOI

• Chronic Electronic Cigarette Exposure Promotes Atherosclerosis and Chondrogenic Modulation of Smooth Muscle Cells

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-09-17

  preprintOpen accessSenior authorCorresponding

  BACKGROUND: Electronic cigarette (E-cig) use has reached epidemic proportions worldwide, yet its cardiovascular consequences remain poorly defined. While several lines of evidences in human epidemiological and animal studies suggest chronic aerosol exposure accelerates atherosclerosis; the cellular and molecular mechanisms underlying this pathological remain unknown. METHODS: We exposed hyperlipidemic mice to chronic e-cigarette aerosol inhalation and characterized the plaque cellular landscape by coupling SMC lineage tracing with single-cell transcriptomic/epigenomic profiling and histologic phenotyping. We subsequently leveraged human coronary artery smooth muscle cells (HCASMCs) to validate in vivo discovery and identified E-cig specific pathological signaling pathways relevant to human vascular disease risk. RESULTS: Chronic E-cig aerosol exposure accelerated atherosclerosis, increasing both SMC phenotypic modulation and plaque macrophage burden in a lipid-independent manner. Transcriptomically, SMCs are particularly more sensitive to E-cig than other vascular cell types. E-cig exposure reprogrammed SMCs toward a pro-calcifying, chondrogenic phenotype, thereby enhancing vascular ossification in vivo and in HCASMCs in vitro. Mechanistically, E-cig mediated SMC fate alteration occurs through activation of a glutamatergic/NMDAR signaling program, that increased NMDAR-dependent Ca2+ influx in a GRIN2A dependent manner. Notably, inhibition of GRIN2A mediated signaling reversed E-cig-induced pathological shifts in SMC phenotype. CONCLUSIONS: SMC chondrogenic reprogramming and subsequent vascular calcification are central to the detrimental cardiovascular consequences of E-cig exposure. Our findings implicate a GRIN2A-dependent glutamatergic/NMDAR signaling axis in SMC as a primary driver of this calcifying remodeling program. These findings define a SMC-specific vulnerability to E-cig aerosols and establish the GRIN2A/NMDAR pathway as potential therapeutic targets for mitigating E-cig-associated cardiovascular disease.

  PublisherOA PDFDOI

Recent grants

• Regulation of Inflammation and Atherosclerosis by TCF21

  NIH · $840k · 2016–2022

Frequent coauthors

• Thomas Quertermous

  74 shared

• François Haddad

  Cardiovascular Institute of the South

  71 shared

• William F. Fearon

  VA Palo Alto Health Care System

  69 shared

• Trieu Nguyen

  Palo Alto University

  61 shared

• Michael P. Fischbein

  Stanford Health Care

  58 shared

• Kegan Moneghetti

  Baker Heart and Diabetes Institute

  54 shared

• Philip A. Beachy

  Stanford University

  53 shared

• Milos Pjanic

  53 shared