About

David H. Jang, MD, MSc, FACMT, is an Assistant Professor of Emergency Medicine and an Attending Physician in the Department of Emergency Medicine at the University of Pennsylvania's Perelman School of Medicine. His clinical expertise is focused on emergency medicine, with additional training in medical toxicology. Dr. Jang's research centers on studying mitochondrial function in acute care illnesses, including sepsis and poisoning, through a translational approach that spans cellular models, animal studies, and clinical settings. His laboratory employs advanced techniques such as the O2k-FluoRespirometer, Western blotting, and confocal microscopy to investigate mitochondrial bioenergetics and develop mitochondrial-directed therapies. His work aims to improve prognostic measures and therapeutic strategies for critical illnesses by understanding the complex interactions of mitochondrial bioenergetics, utilizing models like zebrafish, murine, and porcine, and exploring biomarkers in blood cells. Dr. Jang's research is supported by multiple NIH grants, and he has contributed to the scientific understanding of mitochondrial dysfunction in acute care scenarios.

Research topics

• Anesthesia
• Surgery
• Intensive care medicine
• Medicine
• Cardiology
• Internal medicine

Selected publications

• Dupilumab Improved Work Productivity in Patients with CRSwNP: Results from the Global AROMA Registry

  Journal of Allergy and Clinical Immunology · 2026-02-01

  articleSenior author
  PublisherDOI

• Dose-dependent cerebral metabolic impairment in a swine model of carbon monoxide poisoning

  NeuroToxicology · 2026-04-17

  articleOpen accessSenior authorCorresponding

  Carbon monoxide (CO) poisoning is a leading cause of environmental poisoning in the United States and can impair cellular metabolism through both hypoxia and direct mitochondrial toxicity, particularly via inhibition of cytochrome c oxidase (Complex IV, CIV). In this study, we performed a comprehensive assessment of the cerebral metabolic response to CO exposure in a swine model. Twenty-nine swine (~10 kg) were assigned to three groups: Sham (n = 10), CO 1000 ppm (n = 8), and CO 2000 ppm (n = 11). Animals in the CO groups were exposed to CO for 120 minutes followed by 30 minutes of room air. Cerebral metabolism was assessed using invasive cerebral microdialysis and continuous non-invasive diffuse optical monitoring of cerebral blood flow, oxygenation, and CIV redox state. Following the exposure period, brain tissue was harvested for mitochondrial respiration analysis and western blotting. Severe CO exposure (2000 ppm) produced significant cerebral metabolic impairment, demonstrated by decreased oxidation of cytochrome-c-oxidase, reduced oxygen metabolism, and increased microdialysis markers of metabolic stress including lactate-to-pyruvate ratio and glycerol. In contrast, moderate CO exposure (1000 ppm) resulted in minimal metabolic changes despite elevated carboxyhemoglobin levels. Ex-vivo mitochondrial respirometry also demonstrated impaired mitochondrial respiration in CO-exposed animals. These findings demonstrate greater cerebral metabolic dysfunction with higher CO exposure and suggest that carboxyhemoglobin levels alone may not accurately reflect the degree of cerebral metabolic injury. • Severe CO exposure disrupts cerebral mitochondrial metabolism • Optical monitoring detects metabolic impairment during CO poisoning • Severe CO increases lactate, LPR, and glycerol in cerebral microdialysis • CIV inhibition occurs with high-dose CO exposure • COHb alone does not reflect cerebral metabolic injury

  PublisherDOI

• 1514: HIPPOCAMPAL MITOCHONDRIAL DYSFUNCTION PERSISTS FOR 7 DAYS IN A SWINE PEDIATRIC CARDIAC ARREST MODEL

  Critical Care Medicine · 2025-01-01

  article
  PublisherDOI

• Attenuation of Mitochondrial Dysfunction in a Ventricular Fibrillation Swine Model of Cardiac Arrest Treated with Carbon Monoxide

  SSRN Electronic Journal · 2025-01-01

  preprintOpen accessSenior author
  PublisherDOI

• The application of cell-free DNA methylation patterns in critical illnesses: A protocol paper

  PLoS ONE · 2025-05-12

  articleOpen accessSenior author

  Biomarkers in clinical medicine are typically employed to gauge severity of disease, prognosis and to monitor response to treatment. While various biomarkers have been employed in clinical medicine with variable performance characteristics, the use of cell-free DNA (cfDNA) have gained increased traction as a novel biomarker in a wide range of disease states such as cancer and trauma. While the quantification of cfDNA have been correlated with disease severity, the use of methylation pattens of cfDNA can be used to localize the site of injury that may have implications regarding prognosis and therapeutics. We propose a procedure using samples in a swine model of cardiac arrest where carbon monoxide is being used as a therapeutic to demonstrate our method and feasibility to obtain plasma cfDNA methylation patterns to help identify tissue origin with potential application in critical care medicine.

  PublisherDOI

• Attenuation of mitochondrial dysfunction in a ventricular fibrillation swine model of cardiac arrest treated with carbon monoxide

  Resuscitation · 2025-05-16 · 2 citations

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Timing of inotropic support is associated with mortality in patients with acute decompensated heart failure-associated cardiogenic shock

  Intensive Care Medicine Experimental · 2025-10-31 · 4 citations

  articleOpen access

  BACKGROUND: Inotropic support is often used to improve hemodynamics and organ perfusion in patients with advanced heart failure-related cardiogenic shock (ADHF-CS). We aimed to evaluate the effect of inotrope timing on patient mortality in patients meeting Society for Cardiovascular Angiography and Interventions (SCAI) stage-C criteria within 24 h of hospital presentation. METHODS: We analyzed a local cardiogenic shock database of patients admitted to our cardiovascular intensive care units at the University of Pennsylvania from five emergency departments between 2021 and 2023. Adult patients with left ventricular ejection fraction ≤40% were eligible for inclusion. Patients with hypoperfusion, who met at least one physical, biochemical, and hemodynamic criterion for SCAI-C shock were included. The primary outcome was 28-day mortality. We also compared SCAI criteria and diagnostic examination timing between early and delayed inotropic support groups. RESULTS: A total of 138 out of 623 patients (22%) with cardiogenic shock met inclusion criteria for this study. 28-day mortality was higher in patients who received inotropic therapies ≥8 h after cardiogenic shock onset compared to patients who received earlier support (4-h odds ratio of death (OR) 3.19, 95% CI: 1.34-8.03; 8-h OR: 2.4, 95% CI: 1.09-5.26). 28-day mortality was lower in the early inotrope group (<8 h from shock onset) compared to the delayed (≥8 h) group (15/87; 17% vs. 17/51; 32%, p = 0.031). Patients with early inotropic support more often presented with a cool peripheral exam (34% vs. 16%, p = 0.022) and an initial lactate > 2 mmol/dL (71% vs. 49%, p = 0.009). Delayed inotropic support was associated with hypotension at presentation (84% vs. 57%, p = 0.001), longer time to echocardiography (19 [11-36] vs. 15 [3-24] h, p = 0.053) and time to pulmonary artery catheterization (25 [16-45] vs. 16 [2-46] h, p = 0.042). CONCLUSION: Our findings suggest that inotropic support initiated within 8 h of acute presentation is associated with decreased 28-day mortality for patients with ADHF-related cardiogenic shock. Peripheral perfusion and cardiac output measurement were less frequently quantified within the first 24 h for patients with delayed inotropic support. Using shock classification tools, such as the SCAI shock criteria, may help identify patients with CS, especially in its early stages.

  PublisherOA PDFDOI

• Plasma and Imaging Biomarker Changes Following Rotational and Contusional Models of Traumatic Brain Injury in Adolescent Pigs

  Journal of Neurotrauma · 2025-12-11

  article

  Given the heterogeneity of traumatic brain injury (TBI), the development of a therapeutic strategy has been difficult despite decades of research. To develop an accurate classification system to guide individualized treatment, new protein biomarkers of TBI have been studied. We explored if different subtypes of TBI have unique biomarker profiles and histological findings using four pig models of TBI: moderate rotational injury (100-110 r/s), mild rotational injury (85-95 r/s), moderate contusional injury (8-9 mm), and mild contusional injury (6-7 mm). Among these groups, we identified unique profile of plasma neurofilament light (NFL) and glial fibrillary acidic protein (GFAP): whereas moderate contusion animals had early peak of NFL (2-3 days) and GFAP (1 day), mild contusion animals had delayed peak of NFL (8 days) and GFAP (3 days). Diffusion tensor imaging analysis found reduced fractional anisotropy in corona radiata for contusional injured animals but rotational injured animals showed no significant changes compared to control animals. Histological analysis showed prominent vascular inflammation and axonal injury in the pericontusional cortex in contusional injured animals. In rotational injured animals, prominent axonal injury was found in perivascular white matter. Future studies for mechanistic underpinning of biomarker changes are needed to establish therapeutic targets, predict severity of injury, and determine clinical trial enrollment and therapeutic response.

  PublisherDOI

• Blood Cells as a Cellular Biomarker for Mitochondrial Function in a Experimental Model of Acute Carbon Monoxide Poisoning with Treatment

  Journal of Medical Toxicology · 2025-04-28 · 3 citations

  articleOpen accessSenior author

  Abstract Introduction Carbon monoxide (CO) is a leading cause of environmental poisoning in the United States with substantial mortality and morbidity. The mechanism of CO poisoning is complex and includes hypoxia, inflammation, and mitochondrial dysfunction. Currently both biomarkers and therapies for CO poisoning are limited and require new approaches. Methods Rats (~ 300 g) were divided into four groups of ten rodents per group (exposure): Control (room air), CO-400 (400 ppm), CO-1000 (1000 ppm) and CO-2000 (2000 ppm). Rodents received the assigned exposure through a secured tracheotomy tube over 120 min followed by 30 min of re-oxygenation at room air for a total of 150 min. Five additional rodents in each group were administered a succinate prodrug (NV354) at the start of exposure for the duration of the experiment until the reoxygenation period as separate experiments. Cortical brain tissue and whole blood were obtained for mitochondrial respiration. Stored plasma and snap frozen tissue stored at -80 o C were used to obtain protein quantification with Western Blotting. Results All animals in the Sham, CO-400, and CO-1000 groups survived until the end of the exposure period; no animals in the CO-2000 groups survived the exposure and were counted as attrition. We observed a dose-dependent decrease in key respiratory states in both isolated brain mitochondria and peripheral blood mononuclear cells (PBMCs), and, PBMCs respiration more positively correlated with isolated brain mitochondria when compared to carboxyhemoglobin (COHb). There was no significant difference in mitochondrial respiratory states in animals treated with NV354 compared to the untreated group. Conclusions The primary findings from this study include: (1) A dose-dependent decrease with key respiration states with higher concentrations of CO; (2) PBMCs had a higher correlation to isolated brain mitochondria respiration when compared to COHb; and (3) there was no treatment effect with the use of NV354.

  PublisherOA PDFDOI

• The authors reply

  Critical Care Medicine · 2025-01-01

  articleSenior author
  PublisherDOI

Recent grants

• Development of a Porcine Model of Carbon Monoxide Poisoning to Evaluate Cardiac and Mitochondrial Dysfunction

  NIH · $150k · 2020–2023

• Abnormal Mitochondrial Bioenergetic and Motility Signatures in Human Blood Cells as Indices of Acute Poisoning in Patients

  NIH · $675k · 2018–2021

• Mitochondrial-Directed Therapy in Carbon Monoxide Poisoning

  NIH · $465k · 2020–2024

Frequent coauthors

• David H. Wisner

  328 shared

• Diego Castanares‐Zapatero

  Cliniques Universitaires Saint-Luc

  328 shared

• Pierre‐François Laterre

  Cliniques Universitaires Saint-Luc

  328 shared

• Andrew B. Peitzman

  320 shared

• Lewis S. Nelson

  Rutgers New Jersey Medical School

  178 shared

• Eric M. Massicotte

  University of Toronto

  166 shared

• Mitchell M. Levy

  Brown University

  166 shared

• Todd F. VanderHeiden

  165 shared

Labs

• The Resuscitation Science Center (RSC)PI

Education

• MD, MSc, Emergency Medicine

  University of Pennsylvania

Awards & honors

• R01HL166592 (Jang, PI)
• R21ES031243 (Jang, PI)
• R56HL158696 (Jang, PI)