
Phillip Yang
VerifiedStanford University · Rheumatology
Active 1987–2025
About
Phillip Yang is an Associate Professor of Medicine in the field of Cardiovascular Medicine at Stanford University. He is affiliated with the Center for Artificial Intelligence in Medicine & Imaging (AIMI) at Stanford. His work focuses on integrating artificial intelligence into medical and imaging applications, contributing to advancements in healthcare technology. As a faculty member at Stanford, he is involved in research, education, and collaborative projects aimed at leveraging AI to improve medical diagnostics and treatment.
Research topics
- Political Science
- Medicine
- Pediatrics
- Psychiatry
- Clinical psychology
- Physical therapy
- Internal medicine
- Psychology
- Surgery
Selected publications
Neurology · 2025-04-07 · 3 citations
articleIn this study, we aimed to better understand the duration and severity of autonomic dysfunction in adults with Long COVID (LC) and evaluate its impact on function and quality of life. We also sought to assess risk factors of moderate to severe autonomic dysfunction in LC as well as the risk of developing postural tachycardia syndrome (POTS).
Journal of the American Academy of Child & Adolescent Psychiatry · 2025-10-01
article1st authorCorrespondingCirculation · 2025-11-03
articleSenior authorBackground: Disruption of mitochondrial energy metabolism plays a critical role in the pathophysiology of ischemic heart failure. We previously demonstrated that intramyocardial injection of mitochondria-rich extracellular vesicles (M-EVs) derived from iPSC-cardiomyocytes (iCMs) promotes mitochondrial transfer and biogenesis in recipient cardiomyocytes, leading to improved cardiac function in both acute myocardial infarction (AMI) and chronic heart failure (CHF) porcine models. In this study, we aimed to characterize single-cell transcriptional responses in the peri-infarct region (PIR) of both AMI and CHF models and to identify the cell-type-specific effects of M-EV therapy. Methods: M-EVs were isolated by differential centrifugation from the conditioned medium of human iCMs. Myocardial infarction was induced in Yorkshire pigs by balloon occlusion of the left anterior descending artery (LAD) for 60 minutes (Week 0). In the AMI model, 1.0 × 10 11 M-EVs or PBS were delivered immediately after MI via transendocardial injection into the PIR using a percutaneous catheter system (Biocardia, Inc.). In the CHF model, the same dose was injected into the PIR four weeks post-MI. Cardiac function and scar size were assessed by gadolinium-enhanced cardiac MRI four weeks after treatment. Myocardial tissue samples were collected from the PIR and remote non-ischemic areas for single-nucleus RNA sequencing to analyze transcriptomic changes. Results: Both AMI and CHF models demonstrated significant improvement in LVEF in the M-EV–treated group compared to PBS controls at four weeks post-treatment. No significant differences in scar size were observed. In the AMI model, cardiomyocytes exhibited suppression of mitochondrial metabolism, which was reversed by M-EV–mediated activation of mitochondrial biogenesis, particularly complex I assembly. In contrast, CHF hearts showed transcriptional signatures indicative of altered substrate utilization, and M-EV therapy was associated with upregulation of PDK4-mediated fatty acid oxidation. Conclusion: M-EV therapy improved cardiac function in both acute and chronic porcine MI models through distinct mechanistic pathways. These findings support M-EVs as a novel therapeutic approach that targets cardiac metabolism by restoring mitochondrial function and cellular bioenergetics in a context-dependent manner.
American Journal of Respiratory and Critical Care Medicine · 2025-05-01
articleAbstract Rationale: Pulmonary vascular remodelling is the pathological hallmark of pulmonary arterial hypertension (PAH), but patients ultimately succumb to secondary right ventricular failure (RVF). RV fibrosis is increasingly recognised as a potential therapeutic target in RVF. Previous in vitro work by our group showed that Enzastaurin modulates BMPR2 and the fibroblast-to-myofibroblast transition (FMT), both of which are implicated in PAH pathogenesis. Specifically, we demonstrated that Enzastaurin inhibits TGF-beta-induced Snail expression in vitro. Snail, a transcription factor most commonly associated with epithelial-to-mesenchymal transition (EMT), has also been shown, by our group and others, to be strongly associated with fibroblast activation/FMT. Additionally, we found that snail is expressed early and transiently in the pressure-overloaded RV. Recently, we showed that therapeutic Enzastaurin improved RV function but had negligible effects on RV fibrosis in vivo. Since therapeutic Enzastaurin was administered at a time when cardiac Snail expression peaked in the pulmonary artery banding (PAB) model, one week after PAB, we hypothesized that preventing cardiac Snail expression by prophylactic Enzastaurin, administered prior to PAB, was required to reduce RV fibrosis and improve RV function in the pressure-overloaded RV. Methods: Eighteen-week-old male and female Myh6 (myosin heavy chain 6)MerCreMer-mTmG mice received a single intraperitoneal injection of tamoxifen (0.025mg/100μl), 2 weeks prior to the administration of Enzastaurin (5mg/kg/day; Selleck Chemical LLC, TX) or vehicle control via a subcutaneous Alzet mini-osmotic pump (200μl reservoir; delivery rate, 0.15μl/hour; Cupertino, CA) for 6 weeks. After an initial one-week prophylactic Enzastaurin (or vehicle) treatment, all mice underwent PAB surgery using a 25G needle. Five weeks post-PAB, right and left ventricular (RV/LV) function and RV hypertrophy were assessed using a 3.0T MRI scanner (Signa 3T HDx; GE HealthCare, USA). The percentage of RV fibrosis was assessed by analysing picrosirius red (PSR) and Masson's trichrome (Tri) stains. Results: Prophylactic Enzastaurin significantly reduced the percentage of PAB-induced RV fibrosis compared to the vehicle (mean fibrosis %, 17.57± 2.68 SEM versus 5.92± 1.67 SEM, PSR; 17.64± 2.19 SEM versus 7.49± 2.42 SEM, Tri; n=3-4; p<0.03). Additionally, RV function was mildly improved in the PAB mice that received prophylactic Enzastaurin. Specifically, RV ejection fraction (EF) (%) significantly increased compared to vehicle (mean RV EF%, 60.77± 3.34 versus 73.92± 2.67; n=3-4; p<0.04). Conclusions: Unlike therapeutic Enzastaurin, prophylactic Enzastaurin substantially reduced PAB-induced RV fibrosis, and was associated with improvements in RV EF. These data support a role of Enzastaurin-mediated Snail inhibition as a promising modulator in pressure-overloaded RV failure.
Circulation · 2025-11-03
articleSenior authorIntroduction: Beta blockers, renin-angiotensin-aldosterone antagonists, and mineralocorticoid antagonists are mainstays of current guideline-directed medical therapy (GDMT) in heart failure with reduced left ventricular ejection fraction (LVEF). GDMT has been hypothesized to interact and have protective effects in bioenergetics in cardiac injury by reducing cardiac workload and energy demand. We have previously demonstrated in a human-induced pluripotent stem cell-derived cardiomyocytes (iCMs) hypoxia model that treatment with GDMT plus mitochondrial-rich extracellular vesicles (M-EVs) improves cell viability. Here, we demonstrate the effect of GDMT and M-EV treatment in an established mouse LAD-infarct model. Methods: A total of 16 CD1 mice (50% female and male) underwent left anterior descending artery (LAD) injury, divided into 4 groups plus control (3-4 mice/group after accounting for mortality): PBS sham, metoprolol at 30mg/kg/day, empagliflozin at 10mg/kg/day, M-EVs+ metoprolol, and M-EVs + empagliflozin. 1.0x10 9 M-EVs were directly injected into the peri-infarct region via thoracotomy approach shortly after LAD ligation in the applicable groups. Metoprolol and empagliflozin were administered via daily oral gavage. LV function was assessed by cardiac MRI at week 4 after LAD infarct. M-EVs were collected using differential ultracentrifugation of iCM-conditioned medium. Quality and concentrations are determined via nanoparticle analyzer. Results: The average LV ejection fraction of the normal saline sham group was 29.1%; metoprolol only group 32.2%; empagliflozin only group 32.7%; metoprolol + M-EV group 35.5%; empagliflozin + MEV group 37.2%. There was an 18% overall mortality rate after LAD ligation, all within the first 72 hours after surgery. There was a trend toward significance in the combination medications + M-EV groups. The MRI data is currently being processed for LV viability and scar area. Conclusion: In this initial small sample study of combination therapy of M-EV plus 2 GDMT, there was a trend toward significance in the improvement of mice LVEF after 4 weeks of treatment after LAD ligation. We hypothesize that the results may be from M-EV therapy in conjunction with GDMT, potentially conferring therapeutic benefit by an additive effect of mitochondrial augmentation and a decrease in energy consumption. These results will set up further studies of the additive effect and mechanisms of GDMT and M-EV therapy via multi-omics approaches.
Proceedings on CD-ROM - International Society for Magnetic Resonance in Medicine. Scientific Meeting and Exhibition/Proceedings of the International Society for Magnetic Resonance in Medicine, Scientific Meeting and Exhibition · 2025-09-16
articleSenior authorMotivation: Manganese enhanced MRI has shown promise in differentiating viable from non-viable myocardium, yet its potential for assessing the level of myocardial viability is unexplored. Goal(s): To evaluate whether MEMRI can detect viability differences in rat heart transplant models through dynamic imaging of manganese uptake. Approach: Rat hearts were transplanted either immediately or after 18-hour preservation. MEMRI was performed at three phases post-injection to calculate signal intensity ratios (SIR) in myocardial tissue, comparing changes over time between groups. Results: SIR analysis revealed significant viability-dependent enhancement differences, particularly in late-phase imaging, supporting MEMRI's role in early myocardial viability assessment for transplantation. Impact: This study demonstrates that an increase in signal intensity ratio reflects the level of myocardial viability and highlights MEMRI's potential for assessing myocardial viability in transplant models. This semi-quantitative approach could enhance clinical evaluations of myocardial viability.
Correction: Chronic autonomic symptom burden in long‑COVID: a follow‑up cohort study
Clinical Autonomic Research · 2025-04-24 · 1 citations
erratumOpen accessPublic Health Reports · 2025-01-06 · 4 citations
articleOpen accessOBJECTIVES: Studies suggest that people experiencing housing insecurity and homelessness (HIH) have varying experiences with food insecurity. We estimated the prevalence of food insecurity and identified the factors associated with it among people experiencing HIH in the United States. METHODS: We conducted a meta-analysis of the prevalence of food insecurity among people experiencing HIH and a systematic review of associated factors through a comprehensive search of 8 academic databases. We identified 3398 unique articles and included 40 studies in the review that met the following criteria: included observational or experimental data on the prevalence of food insecurity among people experiencing HIH, conducted in the United States, and written in English. RESULTS: The overall prevalence of food insecurity was 57% (95% CI, 48%-65%). Most people experiencing HIH had food insecurity, and our estimated prevalence among people experiencing HIH was >4 times higher than the prevalence in the US population. Experiencing symptoms of a mental health condition (eg, depression, posttraumatic stress disorder, anxiety) in addition to HIH was most frequently (7 datasets) associated with increased odds of food insecurity. Social and institutional support was most frequently (5 datasets) associated with decreased odds of food insecurity. CONCLUSION: Our findings suggest that multisector coordination is needed to address individual- and system-level factors associated with food insecurity and HIH.
Chronic autonomic symptom burden in long-COVID: a follow-up cohort study
Clinical Autonomic Research · 2025-02-05 · 12 citations
articlePost-COVID-19 Vaccination and Long COVID: Insights from Patient-Reported Data
Vaccines · 2024-12-18 · 6 citations
articleOpen accessIntroduction: COVID-19 vaccinations reduce the severity and number of symptoms for acute SARS-CoV-2 infections and may reduce the risk of developing Long COVID, also known as post-acute sequelae of SARS-CoV-2 (PASC). Limited and heterogenous data exist on how these vaccinations received after COVID-19 infection might impact the symptoms and trajectory of PASC, once persistent symptoms have developed. Methods: We investigated the association of post-COVID-19 vaccination with any SARS-CoV-2 vaccine(s) on PASC symptoms in two independent cohorts: a retrospective chart review of self-reported data from patients (n = 128) with PASC seen in the Stanford PASC Clinic between May 2021 and May 2022 and a 2023 multinational survey assessment of individuals with PASC (n = 484). Findings: Within the PASC Clinic patient cohort (n = 128), 58.6% (n = 75) were female, and 41.4% (n = 53) were male; 50% (n = 64) were white, and 38.3% (n = 49) were non-white. A total of 60.2% (n = 77) of PASC Clinic patients reported no change in their PASC symptoms after vaccination, 17.2% (n = 22) reported improved symptoms, and 22.7% (n = 29) reported worsened symptoms. In the multinational survey cohort (n = 484), 380 were from the U.S., and 104 were from outside the U.S.; 88.4% (n = 428) were female, and 11.6% (n = 56) were male; and 88.8% (n = 430) were white, and 11.2% (n = 54) were non-white. The distribution of survey self-reported vaccine effects on PASC symptoms was 20.2% worsened (n = 98), 60.5% no effect (n = 293), and 19.2% improved (n = 93). In both cohorts, demographic features, including age, sex, and race/ethnicity, were not significantly associated with post-vaccination PASC symptom changes. There was also a non-significant difference in the median dates of COVID-19 infection among the different outcomes. BMI was significant for symptom improvement (p = 0.026) in the PASC Clinic cohort, while a history of booster doses was significant for symptom improvement (p < 0.001) in the survey cohort. Conclusions: Most individuals with PASC did not report significant changes in their overall PASC symptoms following COVID-19 vaccinations received after PASC onset. Further research is needed to better understand the relationship between COVID-19 vaccinations and PASC.
Recent grants
NIH · $255k · 2006
Frequent coauthors
- 72 shared
Micheline Resende
- 64 shared
Jonathan J. Shuster
Florida College
- 64 shared
Joshua M. Hare
University of Miami
- 64 shared
John P. Cooke
Houston Methodist
- 64 shared
Roberto Bolli
University of Louisville
- 64 shared
Doris A. Taylor
- 64 shared
Elizabeth Wise
Johns Hopkins Medicine
- 64 shared
Jay H. Traverse
Abbott Northwestern Hospital
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