Joe GN Garcia
- Professor, Medicine
- Professor, Physiology
- Professor, Internal Medicine
- Professor, Pharmacology and Toxicology
- Professor, Physiological Sciences - GIDP
- Professor, BIO5 Institute
- (520) 626-3151
- AHSC, Rm. 2301
- TUCSON, AZ 85724-5099
- skipgarcia@email.arizona.edu
Biography
Dr. Garcia completed his B.S. in Biology at the University of Dallas in 1976, where he is noted as one of their notable people. He received his M.D. from the University of Texas Southwestern Medical School in 1980.[3] He completed internship and residency training in Internal Medicine at the University of Iowa Hospitals and Clinics (1980–1983) and fellowship training in Pulmonary and Critical Care Medicine at Albany Medical College (1983–1985).
Garcia began his academic career as an Assistant Professor of Medicine at the University of Texas Health Center at Tyler (1985–1988) where he established the first Occupational Lung Center. He was subsequently recruited as an Associate Professor to Indiana University School of Medicine (1988–1998) where (in 1992) he became the youngest endowed full Professor in Indiana University School of Medicine history as the Dr. Calvin H. English Professor of Medicine. He was locally recognized as a staunch advocate for institutional diversity and for his volunteer work and community service with Indiana's Hispanic migrant farm workers. For these efforts, Garcia received the State of Indiana's Otis Bowen Community Service award (1994) and the Physician Community Service Award (1994) from the Indiana State Medical Association.
In 1998, Garcia was recruited to Johns Hopkins University School of Medicine serving in several major academic leadership positions including the Dr. David Marine Professor of Medicine, Environmental Health Sciences and Biomedical Engineering, and the Director of Pulmonary and Critical Care Medicine (1998–2005). During his tenure at Division Director (1998 - 2005), Garcia doubled the number of faculty and grants with considerable diversity, including the expansion of PhDs, women and under-represented minorities. He initiated significant growth and expansion in lung transplantation, pulmonary hypertension, adult cystic fibrosis, health care outcomes, vascular biology, asthma and COPD research.[4] Dr. Garcia was awarded the Levine Excellence in Mentoring Award in 2005.[5] He is also responsible for research growth in the Division level of $2 million/year in NIH funding in 1998 and over $30 million/year and a top national ranking among US academic pulmonary and critical care divisions.
In May 2005 Garcia joined The University of Chicago as the Lowell T. Coggeshall Professor of Medicine and Chairman of the Department of Medicine.[6] During his tenure as chair (2005 - 2009) Garcia led the strategic growth of the University of Chicago's largest department. Under his leadership, research funding exceeded $80 million annually with the Department's national ranking for federal research rising from #25 to #10 (2005 - 2009). While chair, Garcia directed several initiatives improving the gender, racial and ethnic diversity of the Department's faculty and residency fellowship training programs. h[7] With a dedicated focus on junior faculty development and the physician-scientist career pathway, under Garcia's leadership, the department of Medicine experienced a 200% increase in the number of individually awarded NIH career awards (K-Series). Based on the success of these initiatives, in 2006, Garcia was awarded the Diversity Award from the Bowman Society and the Association of Professors of Medicine.[8] Anticipating the push to precision medicine, Garcia established the Section of Genetic Medicine and recruited Nancy Cox, PhD and the first section chief and launched the Translational Research Initiative in the Department of Medicine (TRIDOM).,[9] a large-scale sample collection effort enabling investigators to link clinical information on health and disease status to biological samples.[10]
In February 2010, he was named the Vice Chancellor for Research and Earl M Bane Professor of Medicine at the University of Illinois at Chicago overseeing an almost $400 million research portfolio (70% biomedical research). He launched a broad strategic plan that drove the creation of new institutes and centers focused on precision medicine, health disparities and bioinformatics. In February 2011 Garcia was named the first University of Illinois-Vice President for Health Affairs.[11] Reporting only to the President of the University of Illinois, he oversaw a $1.5 billion enterprise in total annual clinical operating revenues and expenses. He successfully implementd a complete rebranding to form the University of Illinois Hospital and Health Science System, and integrated system that included a University hospital, a VA hospital, over 60 outpatient care clinics, 12 federally, qualified health centers, 7 health science colleges and 4 regional campuses.[12][13] Under his leadership, new health care clinics were opened in Englewood[14] and Brighton Park.[15] He served as the founding Director for the Institute for Personalized Respiratory Medicine which again has a large focus on health disparities.
In December 2010 he founded Aqualung Therapeutics, designed to develop new therapies for the critically ill.[16]
In 2011 he was elected to the Institute of Medicine of the National Academies. (Now known as the National Academy for Medicine)[17]
In 2013, Garcia was recruited to the University of Arizona as the Senior Vice President for Health Sciences and Merlin K. DuVal Endowed Professor of Medicine.[18] Garcia led the strategic integration of undergraduate and graduate education research, service and clinical activities among the UA Health colleges, centers and clinical affiliations.[19] Over the 3.5 year time frame, her served as the Interim Dean, College of Medicine - Tucson (2014 - 2015) ans recruited 3 UA Health Science Deans,[20][21][22] 10 key department chair positions, 10 new associate vice president and center directors and 12 UA division directors as well as number of key scientific leaders in cutting edge research.[23] He recruited Andrew S. Kraft, M.D. to direct the UA NCI-designated Comprehensive Cancer Center[24] and successfully led the renewal of UA's NCI Comprehensive Cancer Center grant (July 2016)[25] Garcia led the re-branding of the Arizona Health Science Center to become the University of Arizona Health Sciences (UAHS) with and integration of UAHS critical services and improvements in cost efficiency.
Academic initiatives included establishment of 4 UAHS thematic centers of excellence in health disparities, population health and health outcomes, precision medicine and neuroscience.[26] The creation of these new centers resulted in increases in NIH funding and the award of a $43.3 million NIH precision medicine initiative cohort program award.[27] Garcia initiated efforts to increase diversity within the five health science colleges creating the Office of Diversity and Inclusion,[28] and fostering such programs as PRIDE, BLAISER and FRONTERA which focus on creating a diverse health-care workforce.[29]
Garcia was the lead member of the UA Health Science (UAHS) negotiation team, helping to facilitate the merger between the University of Arizona Health Network and Phoenix-based Banner Health System. This included creating a $300 million academic endowment to be used at the UA discretion to support research and other academic pursuits, $150 million to clear UAHN debt and $500 million in capital improvements over five years.[30]
In January 2017, Garcia changed his focus to continuing his innovative clinical and translational research[31] and to serve as Founder and CEO of Aqualung Therapeutics and Restore Therapeutics, companies focused on the high mortality rate in clinical illnesses.
Work Experience
- Graduate Faculty, Indiana University School of Medicine (1989 - 1998)
Interests
No activities entered.
Courses
2018-19 Courses
-
Dissertation
PS 920 (Spring 2019) -
Dissertation
CTS 920 (Fall 2018) -
Dissertation
PS 920 (Fall 2018) -
Independent Study
PSIO 399 (Fall 2018) -
Introduction to Research
MCB 795A (Fall 2018) -
Senior Capstone
MCB 498 (Fall 2018) -
Thesis
CTS 910 (Fall 2018)
2017-18 Courses
-
Directed Rsrch
MCB 392 (Spring 2018) -
Dissertation
CTS 920 (Spring 2018) -
Dissertation
PS 920 (Spring 2018) -
Directed Rsrch
MCB 392 (Fall 2017) -
Dissertation
CTS 920 (Fall 2017)
2016-17 Courses
-
Dissertation
CTS 920 (Summer I 2017) -
Dissertation
CTS 920 (Spring 2017) -
Individualized Science Writing
CTS 585 (Spring 2017)
Scholarly Contributions
Journals/Publications
- Black, S., Yuan, J., Garcia, A. N., Jacobson, J. R., Garcia, J. G., Wu, X., Zemskov, E., Desai, A., Gross, C., & Wang, T. (2017). Endothelial cell signaling and ventilator-induced lung injury: molecular mechanisms, genomic analyses, and therapeutic targets. American journal of physiology. Lung cellular and molecular physiology, 312(4), L452-L476.More infoMechanical ventilation is a life-saving intervention in critically ill patients with respiratory failure due to acute respiratory distress syndrome (ARDS). Paradoxically, mechanical ventilation also creates excessive mechanical stress that directly augments lung injury, a syndrome known as ventilator-induced lung injury (VILI). The pathobiology of VILI and ARDS shares many inflammatory features including increases in lung vascular permeability due to loss of endothelial cell barrier integrity resulting in alveolar flooding. While there have been advances in the understanding of certain elements of VILI and ARDS pathobiology, such as defining the importance of lung inflammatory leukocyte infiltration and highly induced cytokine expression, a deep understanding of the initiating and regulatory pathways involved in these inflammatory responses remains poorly understood. Prevailing evidence indicates that loss of endothelial barrier function plays a primary role in the development of VILI and ARDS. Thus this review will focus on the latest knowledge related to 1) the key role of the endothelium in the pathogenesis of VILI; 2) the transcription factors that relay the effects of excessive mechanical stress in the endothelium; 3) the mechanical stress-induced posttranslational modifications that influence key signaling pathways involved in VILI responses in the endothelium; 4) the genetic and epigenetic regulation of key target genes in the endothelium that are involved in VILI responses; and 5) the need for novel therapeutic strategies for VILI that can preserve endothelial barrier function.
- Desai, A., Choi, B., Dudley, S. C., Kittles, R., Machado, R. F., Garcia, J. G., Hillery, C., Indik, J. H., Goldman, S., Juneman, E. B., Groth, J., Nair, N., Rutledge, C., Kanady, J., Fleming, I., Batai, K., Weigand, K., Shi, G., Kim, T. Y., , Gupta, G., et al. (2018). IL-18 is a novel mediator of prolonged QTc and ventricular arrhythmias associated with Sickle Cell Disease. Proceedings of the National Academy of Sciences.
- Hecker, L., Garcia, J. G., Wang, T., Colson, B., Knox, A., Mohamed, M., Quijada, H., Desai, A., Ahmad, K., Shin, Y. J., & Palumbo, S. (2017). Dysregulated Nox4 ubiquitination contributes to redox imbalance and age-related severity of acute lung injury. American journal of physiology. Lung cellular and molecular physiology, 312(3), L297-L308.More infoAcute respiratory distress syndrome (ARDS) is a devastating critical illness disproportionately affecting the elderly population, with both higher incidence and mortality. The integrity of the lung endothelial cell (EC) monolayer is critical for preservation of lung function. However, mechanisms mediating EC barrier regulation in the context of aging remain unclear. We assessed the severity of acute lung injury (ALI) in young (2 mo) and aged (18 mo) mice using a two-hit preclinical model. Compared with young cohorts, aged mice exhibited increased ALI severity, with greater vascular permeability characterized by elevated albumin influx and levels of bronchoalveolar lavage (BAL) cells (neutrophils) and protein. Aged/injured mice also demonstrated elevated levels of reactive oxygen species (ROS) in the BAL, which was associated with upregulation of the ROS-generating enzyme, Nox4. We evaluated the role of aging in human lung EC barrier regulation utilizing a cellular model of replicative senescence. Senescent EC populations were defined by increases in β-galactosidase activity and p16 levels. In response to lipopolysaccharide (LPS) challenge, senescent ECs demonstrate exacerbated permeability responses compared with control "young" ECs. LPS challenge led to a rapid induction of Nox4 expression in both control and senescent ECs, which was posttranslationally mediated via the proteasome/ubiquitin system. However, senescent ECs demonstrated deficient Nox4 ubiquitination, resulting in sustained expression of Nox4 and alterations in cellular redox homeostasis. Pharmacological inhibition of Nox4 in senescent ECs reduced LPS-induced alterations in permeability. These studies provide insight into the roles of Nox4/senescence in EC barrier responses and offer a mechanistic link to the increased incidence and mortality of ARDS associated with aging.
- Yuan, J., Makino, A., Garcia, J. G., Mcdermott, K. M., Rischard, F., Desai, A., Black, S., Khalpey, Z. I., Cordery, A. G., Sun, X., Tang, H., Babicheva, A., Dash, S., Yamamura, H., Yamamura, A., Ayon, R. J., & Song, S. (2017). Capsaicin-induced Ca2+ signaling is enhanced via upregulated TRPV1 channels in pulmonary artery smooth muscle cells from patients with idiopathic PAH. American journal of physiology. Lung cellular and molecular physiology, 312(3), L309-L325.More infoCapsaicin is an active component of chili pepper and a pain relief drug. Capsaicin can activate transient receptor potential vanilloid 1 (TRPV1) channels to increase cytosolic Ca2+ concentration ([Ca2+]cyt). A rise in [Ca2+]cyt in pulmonary artery smooth muscle cells (PASMCs) is an important stimulus for pulmonary vasoconstriction and vascular remodeling. In this study, we observed that a capsaicin-induced increase in [Ca2+]cyt was significantly enhanced in PASMCs from patients with idiopathic pulmonary arterial hypertension (IPAH) compared with normal PASMCs from healthy donors. In addition, the protein expression level of TRPV1 in IPAH PASMCs was greater than in normal PASMCs. Increasing the temperature from 23 to 43°C, or decreasing the extracellular pH value from 7.4 to 5.9 enhanced capsaicin-induced increases in [Ca2+]cyt; the acidity (pH 5.9)- and heat (43°C)-mediated enhancement of capsaicin-induced [Ca2+]cyt increases were greater in IPAH PASMCs than in normal PASMCs. Decreasing the extracellular osmotic pressure from 310 to 200 mOsmol/l also increased [Ca2+]cyt, and the hypo-osmolarity-induced rise in [Ca2+]cyt was greater in IPAH PASMCs than in healthy PASMCs. Inhibition of TRPV1 (with 5'-IRTX or capsazepine) or knockdown of TRPV1 (with short hairpin RNA) attenuated capsaicin-, acidity-, and osmotic stretch-mediated [Ca2+]cyt increases in IPAH PASMCs. Capsaicin induced phosphorylation of CREB by raising [Ca2+]cyt, and capsaicin-induced CREB phosphorylation were significantly enhanced in IPAH PASMCs compared with normal PASMCs. Pharmacological inhibition and knockdown of TRPV1 attenuated IPAH PASMC proliferation. Taken together, the capsaicin-mediated [Ca2+]cyt increase due to upregulated TRPV1 may be a critical pathogenic mechanism that contributes to augmented Ca2+ influx and excessive PASMC proliferation in patients with IPAH.
- Desai, A., Black, S., Wang, T., Garcia, J. G., Sun, X., Adyshev, D., Kelly, G. T., Camp, S. M., & Elangovan, V. R. (2016). Endotoxin- and mechanical stress-induced epigenetic changes in the regulation of the nicotinamide phosphoribosyltransferase promoter. Pulmonary circulation, 6(4), 539-544.More infoMechanical ventilation, a lifesaving intervention for patients with acute respiratory distress syndrome (ARDS), also unfortunately contributes to excessive mechanical stress and impaired lung physiological and structural integrity. We have elsewhere established the pivotal role of increased nicotinamide phosphoribosyltransferase (NAMPT) transcription and secretion as well as its direct binding to the toll-like receptor 4 (TLR4) in the progression of this devastating syndrome; however, regulation of this critical gene in ventilator-induced lung injury (VILI) is not well characterized. On the basis of an emerging role for epigenetics in enrichment of VILI and CpG sites within the NAMPT promoter and 5'UTR, we hypothesized that NAMPT expression and downstream transcriptional events are influenced by epigenetic mechanisms. Concomitantly, excessive mechanical stress of human pulmonary artery endothelial cells or lipopolysaccharide (LPS) treatment led to both reduced DNA methylation levels in the NAMPT promoter and increased gene transcription. Histone deacetylase inhibition by trichostatin A or Sirt-1-silencing RNA attenuates LPS-induced NAMPT expression. Furthermore, recombinant NAMPT administration induced TLR4-dependent global H3K9 hypoacetylation. These studies suggest a complex epigenetic regulatory network of NAMPT in VILI and ARDS and open novel strategies for combating VILI and ARDS.
- Sun, X., Elangovan, V. R., Shimizu, Y., Ma, S. F., Wang, T., & Garcia, J. G. (2016). Genetic and Epigenetic Regulation of Myosin Light Chain Kinase by Inflammatory Lung Disease Associated Polymorphisms. Journal of Investigative Medicine.
- Wang, T., Garcia, J. G., & Zhang, W. (2012). Epigenetic Regulation in Particulate Matter-Mediated Cardiopulmonary Toxicities: A Systems Biology Perspective. Current pharmacogenomics and personalized medicine, 10(4), 314-321.More infoParticulate matter (PM) air pollution exerts significant adverse health effects in global populations, particularly in developing countries with extensive air pollution. Understanding of the mechanisms of PM-induced health effects including the risk for cardiovascular diseases remains limited. In addition to the direct cellular physiological responses such as mitochondrial dysfunction and oxidative stress, PM mediates remarkable dysregulation of gene expression, especially in cardiovascular tissues. The PM-mediated gene dysregulation is likely to be a complex mechanism affected by various genetic and non-genetic factors. Notably, PM is known to alter epigenetic markers (e.g., DNA methylation and histone modifications), which may contribute to air pollution-mediated health consequences including the risk for cardiovascular diseases. Notably, epigenetic changes induced by ambient PM exposure have emerged to play a critical role in gene regulation. Though the underlying mechanism(s) are not completely clear, the available evidence suggests that the modulated activities of DNA methyltransferase (DNMT), histone acetylase (HAT) and histone deacetylase (HDAC) may contribute to the epigenetic changes induced by PM or PM-related chemicals. By employing genome-wide epigenomic and systems biology approaches, PM toxicogenomics could conceivably progress greatly with the potential identification of individual epigenetic loci associated with dysregulated gene expression after PM exposure, as well the interactions between epigenetic pathways and PM. Furthermore, novel therapeutic targets based on epigenetic markers could be identified through future epigenomic studies on PM-mediated cardiopulmonary toxicities. These considerations collectively inform the future population health applications of genomics in developing countries while benefiting global personalized medicine at the same time.
- Singleton, P. A., Mambetsariev, N., Lennon, F. E., Mathew, B., Siegler, J. H., Moreno-Vinasco, L., Salgia, R., Moss, J., & Garcia, J. G. (2010). Methylnaltrexone potentiates the anti-angiogenic effects of mTOR inhibitors. Journal of angiogenesis research, 2(1), 5.More infoRecent cancer therapies include drugs that target both tumor growth and angiogenesis including mammalian target of rapamycin (mTOR) inhibitors. Since mTOR inhibitor therapy is associated with significant side effects, we examined potential agents that can reduce the therapeutic dose.
Presentations
- Yuan, J., Garcia, J. G., Desai, A., & Rischard, F. (2017, May). Right ventriculo-arterial physiologic and morphologic phenotyping in Hispanic and non-Hispanic cohorts (PVDOMICS). American Thoracic Society Conference. Washington, D.C.: American Thoracic Society.
Poster Presentations
- Berghout, J., Casanova, N., Lussier, Y. A., Gonzalez-Garay, M. L., Pouladi, N., Navarrete, J., Garcia, J. G., Knox, K. S., Knox, K. S., Garcia, J. G., Pouladi, N., Navarrete, J., Gonzalez-Garay, M. L., Lussier, Y. A., Casanova, N., & Berghout, J. (2017, May). TNF-α specific PBMC responses in complicated and uncomplicated sarcoidosis by RNA-Seq. American Thoracic Society International Conference. Washington DC: ATS.
- Casanova, N., Gonzalez-Garay, M. L., Pouladi, N., Knox, K. S., Garcia, J. G., Navarrete, J., Lussier, Y. A., & Berghout, J. (2017, May). TNF-α specific PBMC responses in complicated and uncomplicated sarcoidosis by RNA-Seq. American Thoracic Society International Conference. Washington DC: ATS.
- Desai, A., Bedrick, E. J., Black, S., Makino, A., Yuan, J., Garcia, J. G., Rischard, F., Kadakia, A., Patel, K., Austin, E. D., Hemnes, A. R., Brittain, E. L., Dherange, P., Trutter, L., Natarajan, B., Sinari, S., Whitaker, M. E., & Nair, V. (2017, May). Effects of diabetes mellitus on pulmonary vascular stiffness and right ventricular remodeling. American Thoracic Society Conference. Washington, D.C.: American Thoracic Society.
- Desai, A., Desai, A., Kittles, R., Kittles, R., Nichols, W. C., Nichols, W. C., Paucilio, M. W., Paucilio, M. W., Yuan, J., Yuan, J., Garcia, J. G., Garcia, J. G., Nair, V., Nair, V., Steiner, H., Steiner, H., Kaye, J., Kaye, J., Arora, A., , Arora, A., et al. (2017, November). Genome-Wide Association Study of Vasodilator Response in Pulmonary Arterial Hypertension. American Heart Association Scientific Sessions. Anaheim, CA: AHA.More infoLate Breaking AbstractCirculation. 2017; 136: A24015
- Desai, A., Kittles, R., Nichols, W. C., Pauciulo, M. W., Yuan, J., Garcia, J. G., Nair, V., Steiner, H. E., Kaye, J. B., Arora, A., Batai, K., & Karnes, J. H. (2017, November). Genome-wide association of vasodilator drug response in pulmonary arterial hypertension.. American Heart Association Scientific Sessions. Anaheim, CA: American Heart Association.
- Desai, A., Yuan, J., Garcia, J. G., Rischard, F., Duarte, J., Larson, B., Knox, K., Kadakia, A., Patel, K., Cordery, A., Gupta, G., Nair, V., Lynn, H. D., & Gupta, A. (2017, May). Exome sequencing reveals a novel SNP in UCHL1 in pulmonary arterial hypertension.. American Thoracic Society Conference.. Washington, D.C.: American Thoracic Society.
- Desai, A., Yuan, J., Rischard, F., Garcia, J. G., Black, S., Suryanarayana, P., Khalpey, Z. I., Knox, K., Patel, K., Yarlagadda, V., Shewale, A., Riaz, I., Whitaker, M., Dhrange, P., Nair, V., & Natarajan, B. (2017, June). Hispanic disparities in PAH: Multi-modality validation of increased susceptibility to right ventricular dysfunction. Arizona Chapter of American College of Cardiology. Phoenix, AZ: Arizona Chapter of American College of Cardiology.
- Desai, A., Garcia, J. G., Yuan, J., Jacobson, J. J., Nair, V., Mitra, S., Tang, H., Gupta, G., & Gupta, A. (2016, May). Gadd45a deficiency attenuates hypoxic pulmonary hypertension via inhibition of ubiquitin carboxyl-terminal esterase L1, UCHL1.. American Thoracic Society Conference. San Francisco, CA: American Thoracic Society.
- Desai, A., Yuan, J., Garcia, J. G., Larson, B. F., Knox, K. S., Sprissler, R., Cordery, A., Gupta, A., Nair, V., & Lynn, H. D. (2016, November). Exome sequencing reveals a novel SNP in TRPC6 in pulmonary arterial hypertension. American Heart Association Scientific Sessions. New Orleans, LA: American Heart Association.
- Desai, A., Yuan, J., Rischard, F., Garcia, J. G., Black, S., Suryanarayana, P., Khalpey, Z. I., Knox, K. S., Patel, K., Yarlagadda, V., Shewale, A., Riaz, I., Whitaker, M., Dherange, P., Nair, V., Natarajan, B., Desai, A., Yuan, J., Rischard, F., , Garcia, J. G., et al. (2016, November). Hispanic disparities in PAH: Multi-modality validation of increased susceptibility to right ventricular dysfunction.. American Heart Association Scientific Sessions;. New Orleans, L: American Heart Association.
- Garcia, J. G., Knox, K. S., Zhou, T., & Casanova, N. (2016, May). Peripheral Blood MicroRNA Signature Differentiates Sarcoidosis. American Thoracic Society International Conference. San Francisco: ATS.
- Desai, A., Garcia, J. G., Yuan, J., Hansen, L., Rischard, F., Suryanarayana, P., Khalpey, Z. I., Knox, K. S., Chinthammit, C., Yarlagadda, V., Whitaker, M. E., Shewale, A., Irbaz Bin Riaz, F., Nair, V., & Dherange, P. (2015, August). Disparities in pulmonary arterial hypertension: Effects of Hispanic ethnicity on susceptibility to right ventricular dysfunction. 2015 American College of Physicians Meeting (ACP). Phoenix, AZ: American College of Physicians.
- Patel, A. R., Lang, R. M., Garcia, J. G., Turner, K., Artz, N., Trevino, S., Ahmad, H., Desai, A., Thiruvoipati, T., & Czobor, P. (2011, Fall). Sickle cell disease associated abnormal aortic stiffness despite absence of systemic hypertension. American Heart Association Scientific Sessions. Orlando, FL: American Heart Association.
Others
- Babicheva, A., Mcdermott, K. M., Ayon, R., Dash, S., Tang, H., Cordery, A. G., Desai, A., Black, S., Garcia, J. G., Makino, A., Yuan, J., Babicheva, A., Mcdermott, K. M., Ayon, R., Dash, S., Tang, H., Cordery, A. G., Desai, A., Black, S., , Garcia, J. G., et al. (2016, October). Role of endothelial-to-mesenchymal transition associated with PHD2/HIF1α/2α pathway in the progression of idiopathic pulmonary arterial hypertension. Arizona Physiological Society meeting.
- Babivheva, A., Mcdermott, K. M., Sun, S., Song, S., Tang, H., Cordery, A. G., Desai, A., Black, S., Garcia, J. G., Makino, A., & Yuan, J. (2016, June). Inhibition of PHD2 Induces Endothelial-to-Mesenchymal Transition in Pulmonary Vascular Endothelial Cells..
