About

David M. Eckmann, PhD, MD, is an Emeritus Professor of Anesthesiology and Critical Care at the University of Pennsylvania. He serves as an Attending Physician in the Department of Anesthesiology & Critical Care at the Hospital of the University of Pennsylvania. Dr. Eckmann is a member of the Institute for Medicine and Engineering, the Institute for Translational Medicine and Therapeutics, and the Cardiovascular Institute at the University of Pennsylvania. He also holds a secondary appointment as Professor of Bioengineering and is an Adjunct Investigator at the University of Pennsylvania Institute for Environmental Medicine, as well as a member of the Nano/Bio Interface Center. His research interests focus on cardiovascular science, specifically cellular metabolic engineering, nanocarrier design for targeted vascular drug delivery, and biomimetic macromolecular surface grafting to improve biocompatibility and reduce bioresponses of vascular biomaterials. Dr. Eckmann has been continuously funded for over 20 years by agencies such as NIH, NSF, Department of Defense, NASA, and private foundations. His work aims to understand mitochondrial function and cellular bioenergetics in relation to cellular mechanical dysfunction, optimize nanocarrier design for vascular drug targeting, and develop biomimetic surface coatings for vascular devices to enhance their biocompatibility and resistance to bacterial biofilm formation.

Research topics

• Medicine
• Materials science
• Chemistry
• Mechanics
• Biophysics

Selected publications

• Proceedings from the 2025 Midwest Pediatric Device Consortium showcase featuring software as a medical device

  BMC Proceedings · 2026-05-10

  articleOpen access

  On July 9, 2025, the Midwest Pediatric Device Consortium hosted its second showcase at the MidTown Collaboration Center in Cleveland, OH. This meeting convened clinicians, engineers, regulators, entrepreneurs, and policy stakeholders to discuss the challenges and opportunities in pediatric medical device development. The program included expert panel discussions addressing value demonstration in healthcare, data-driven post market surveillance, cybersecurity risk and data protection, artificial intelligence, clinical algorithms, and pediatric-specific considerations. This culminated in a pitch competition focused on Software as a Medical Device. This manuscript provides a descriptive summary of the meeting proceedings and synthesizes themes that emerged from panel discussions. The themes underscored the persistent structural barriers in pediatric device development, including alignment of value across stakeholders, limitations of real-world evidence infrastructure, data security challenges, and complexities in artificial intelligence driven technologies. These proceedings are intended to inform clinicians, innovators, and policymakers engaged in pediatric medical device development rather than serve as a formal program evaluation.

  PublisherDOI

• Gas Embolism: Fundamentals, Diagnosis, and Treatment

  IEEE Reviews in Biomedical Engineering · 2026-01-01

  article

  Invasive medical interventions or abrupt reductions in ambient pressure can result in intravascular gas embolism. The accumulation of gas bubbles initiates a cascade of pathophysiological phenomena progressing from platelet activation to ischemia and neurological dysfunction. This review integrates current knowledge of the biophysical mechanisms of bubble nucleation, progression, and vascular occlusion into a framework aligned with the adverse physiological consequences on circulation. The discussion further addresses the present state of clinical practice, diagnostic approaches, and therapeutic interventions. Initial studies on gas embolism utilized in vivo models, and recent in vitro and in silico platforms have provided reproducible and cost-efficient experimental approaches. The initial symptoms of gas embolism often overlap with stroke, myocardial infarction, or sepsis. Reliable detection of intravascular gas bubbles is constrained by the sensitivity, resolution, and accessibility of existing imaging modalities, particularly in systemic cases. Current treatment frameworks emphasize hyperbaric oxygen therapy, while adjunct pharmacological strategies to improve clinical outcomes are under investigation. The challenges responsible for the persistent neglect of gas embolism in both clinical and academic contexts are discussed, and a forward-looking perspective on strategies to overcome these barriers is presented.

  PublisherDOI

• Caffeine, MitoQ, and GABA Prophylaxis of Mitochondrial Dysfunction Induced in Human Pulmonary Cells by Normobaric–Hyperoxia and Hyperbaric–Hyperoxia

  Oxidative Medicine and Cellular Longevity · 2025-01-01 · 1 citations

  articleOpen accessSenior authorCorresponding

  Exposure to hyperoxia lasting either a few days at normobaria or a few hours at hyperbaria induces pulmonary oxygen toxicity. Cellular functional changes resulting from oxygen toxicity include alterations in both mitochondrial dynamics and bioenergetics. The primary goal of this study was to quantify the prophylactic effects of three compounds, caffeine, MitoQ, and γ‐aminobutyric acid (GABA), to protect human pulmonary cells in vitro from mitochondrial alterations induced by normobaric‐ and hyperbaric–hyperoxic conditions. Using cultured lung microvascular and pulmonary artery endothelial cells as well as A549 cells, we examined mitochondrial dynamic and bioenergetics function following exposure to normobaric–hyperoxic (5% CO 2 and 95% O 2 for 72 h) and hyperbaric–hyperoxic (~5% CO 2 equivalent and remainder O 2 at pressure of 4.8 atmosphere absolute (ATA) for 4 h) conditions in the presence of the drugs. Mitochondrial respiration parameters, inner membrane potential, motility, intracellular distribution, and size were measured, along with quantitation of respiration complex levels. Redistribution of intracellular ATP‐linked respiration was determined. Comparisons of results were made to controls under normobaric–normoxic conditions. Effects of the drugs under control conditions were also measured. Presence of the drugs resulted in differential effects on hyperoxia‐induced alterations in cellular respiration function, stability of mitochondrial potential, and distribution of ATP‐linked respiration within the cell. Inclusion of these drugs also produced unique signatures for respiration complex protein levels. Moreso for caffeine than for MitoQ and GABA, its inclusion in the face of hyperoxic exposure served to preserve mitochondrial bioenergetics function, primarily by promoting intracellular redistribution of mitochondrial volume to the perinuclear space. These results indicate a potential role for pharmacologic prophylaxis via therapeutics targeted to support mitochondrial function as a means of protecting the lung from hyperoxia‐induced pulmonary cellular oxygen toxicity.

  PublisherOA PDFDOI

• Hyperbaric oxygen rapidly produces intracellular bioenergetics dysfunction in human pulmonary cells

  Chemico-Biological Interactions · 2024-10-18 · 4 citations

  articleSenior authorCorresponding
  PublisherDOI

• RAB7 deficiency impairs pulmonary artery endothelial function and promotes pulmonary hypertension

  bioRxiv (Cold Spring Harbor Laboratory) · 2023-02-03 · 2 citations

  preprintOpen access

  Pulmonary arterial hypertension (PAH) is a devastating and progressive disease with limited treatment options. Endothelial dysfunction plays a central role in development and progression of PAH, yet the underlying mechanisms are incompletely understood. The endosome-lysosome system is important to maintain cellular health and the small GTPase RAB7 regulates many functions of this system. Here, we explored the role of RAB7 in endothelial cell (EC) function and lung vascular homeostasis. We found reduced expression of RAB7 in ECs from PAH patients. Endothelial haploinsufficiency of RAB7 caused spontaneous PH in mice. Silencing of RAB7 in ECs induced broad changes in gene expression revealed via RNA sequencing and RAB7 silenced ECs showed impaired angiogenesis, expansion of a senescent cell fraction, combined with impaired endolysosomal trafficking and degradation, which suggests inhibition of autophagy at the pre-degradation level. Further, mitochondrial membrane potential and oxidative phosphorylation were decreased, and glycolysis was enhanced. Treatment with the RAB7 activator ML-098 reduced established PH in chronic hypoxia/SU5416 rats. In conclusion, we demonstrate here for the first time the fundamental impairment of EC function by loss of RAB7 that leads to PH and show RAB7 activation as a potential therapeutic strategy in a preclinical model of PH.

  PublisherOA PDFDOI

• RAB7 deficiency impairs pulmonary artery endothelial function and promotes pulmonary hypertension

  Journal of Clinical Investigation · 2023-11-28 · 33 citations

  articleOpen access

  Pulmonary arterial hypertension (PAH) is a devastating and progressive disease with limited treatment options. Endothelial dysfunction plays a central role in the development and progression of PAH, yet the underlying mechanisms are incompletely understood. The endosome-lysosome system is important to maintain cellular health, and the small GTPase RAB7 regulates many functions of this system. Here, we explored the role of RAB7 in endothelial cell (EC) function and lung vascular homeostasis. We found reduced expression of RAB7 in ECs from patients with PAH. Endothelial haploinsufficiency of RAB7 caused spontaneous pulmonary hypertension (PH) in mice. Silencing of RAB7 in ECs induced broad changes in gene expression revealed via RNA-Seq, and RAB7-silenced ECs showed impaired angiogenesis and expansion of a senescent cell fraction, combined with impaired endolysosomal trafficking and degradation, suggesting inhibition of autophagy at the predegradation level. Furthermore, mitochondrial membrane potential and oxidative phosphorylation were decreased, and glycolysis was enhanced. Treatment with the RAB7 activator ML-098 reduced established PH in rats with chronic hypoxia/SU5416. In conclusion, we demonstrate for the first time to our knowledge the fundamental impairment of EC function by loss of RAB7, causing PH, and show RAB7 activation to be a potential therapeutic strategy in a preclinical model of PH.

  PublisherOA PDFDOI

• Hyperoxic exposure alters intracellular bioenergetics distribution in human pulmonary cells

  Life Sciences · 2023-06-24 · 3 citations

  articleSenior authorCorresponding
  PublisherDOI

• Mitochondrial dynamics involves molecular and mechanical events in motility, fusion and fission

  Frontiers in Cell and Developmental Biology · 2022-10-19 · 73 citations

  reviewOpen accessSenior authorCorresponding

  Mitochondria are cell organelles that play pivotal roles in maintaining cell survival, cellular metabolic homeostasis, and cell death. Mitochondria are highly dynamic entities which undergo fusion and fission, and have been shown to be very motile in vivo in neurons and in vitro in multiple cell lines. Fusion and fission are essential for maintaining mitochondrial homeostasis through control of morphology, content exchange, inheritance of mitochondria, maintenance of mitochondrial DNA, and removal of damaged mitochondria by autophagy. Mitochondrial motility occurs through mechanical and molecular mechanisms which translocate mitochondria to sites of high energy demand. Motility also plays an important role in intracellular signaling. Here, we review key features that mediate mitochondrial dynamics and explore methods to advance the study of mitochondrial motility as well as mitochondrial dynamics-related diseases and mitochondrial-targeted therapeutics.

  PublisherOA PDFDOI

• Hydrodynamics and Interfacial Surfactant Transport in Vascular Gas Embolism

  Journal of Heat Transfer · 2021-04-20 · 3 citations

  article1st authorCorresponding

  Abstract Vascular gas embolism—bubble entry into the blood circulation - is pervasive in medicine, including over 340,000 cardiac surgery patients in the U.S. annually. The gas–liquid interface interacts directly with constituents in blood, including cells and proteins, and with the endothelial cells lining blood vessels to provoke a variety of undesired biological reactions. Surfactant therapy, a potential preventative approach, is based on fluid dynamics and transport mechanics. Herein we review literature relevant to the understanding the key gas–liquid interface interactions inciting injury at the molecular, organelle, cellular, and tissue levels. These include clot formation, cellular activation, and adhesion events. We review the fluid physics and transport dynamics of surfactant-based interventions to reduce tissue injury from gas embolism. In particular, we focus on experimental research and computational and numerical approaches involving how surface-active chemical-based intervention. This is based on surfactant competition with blood-borne or cell surface-borne macromolecules for surface occupancy of gas–liquid interfaces to alter cellular mechanics, mechanosensing, and signaling coupled to fluid stress exposures occurring in gas embolism. We include a new analytical approach for which an asymptotic solution to the Navier–Stokes equations coupled to the convection-diffusion interaction for a soluble surfactant provides additional insight regarding surfactant transport with a bubble in non-Newtonian fluid.

  PublisherDOI

• Biophysical Considerations in the Rational Design and Cellular Targeting of Flexible Polymeric Nanoparticles

  Advanced Materials Interfaces · 2021-11-11 · 5 citations

  articleOpen accessCorresponding

  How nanoparticle (NP) mechanical properties impact multivalent ligand-receptor-mediated binding to cell surfaces, the avidity, propensity for internalization, and effects due to crowding remains unknown or unquantified. Through computational analyses, the effects of NP composition from soft, deformable NPs to rigid spheres, effect of tethers, the crowding of NPs at the membrane surface, and the cell membrane properties such as cytoskeletal interactions are addressed. Analyses of binding mechanisms of three distinct NPs that differ in type and rigidity (core-corona flexible NP, rigid NP, and rigid-tethered NP) but are otherwise similar in size and ligand surface density are reported; moreover, for the case of flexible NP, NP stiffness is tuned by varying the internal crosslinking density. Biophysical modeling of NP binding to membranes together with thermodynamic analysis powered by free energy calculations is employed, and it is shown that efficient cellular targeting and uptake of NP functionalized with targeting ligand molecules can be shaped by factors including NP flexibility and crowding, receptor-ligand binding avidity, state of the membrane cytoskeleton, and curvature inducing proteins. Rational design principles that confer tension, membrane excess area, and cytoskeletal sensing properties to the NP which can be exploited for cell-specific targeting of NP are uncovered.

  PublisherOA PDFDOI

Recent grants

• NIH Grant R01HL060230

  NIH · $4.0M · 2013

• NIH Grant R01HL067986

  NIH · $2.4M · 2011

• NIH Grant R01EB006818

  NIH · $3.3M · 2018

• NIH Grant U01EB016027

  NIH · $2.7M · 2019

Frequent coauthors

• P. S. Ayyaswamy

  University of California, Los Angeles

  90 shared

• Ravi Radhakrishnan

  University of Pennsylvania

  67 shared

• Vladimir R. Muzykantov

  Translational Therapeutics (United States)

  58 shared

• Russell J. Composto

  University of Pennsylvania

  51 shared

• Jacob W. Myerson

  California University of Pennsylvania

  20 shared

• Judith Kandel

  University of Pennsylvania

  20 shared

• David H. Jang

  American College of Medical Toxicology

  19 shared

• Samaneh Farokhirad

  19 shared