Idell, Steven, M.D., Ph.D.

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Vice President for Research

Temple Univ. School of Medicine, M.D., 1977
Temple Univ. School of Medicine, Ph.D., 1978


  • Sept 1986-Sept 1991 Recipient, Clinical Investigator Award K08HL01603, National Institutes of Health N.H.L.B.I.
  • Sept 1996-Present Appointed Chair Holder, Temple Chair in Idiopathic Pulmonary Fibrosis. The first endowed chair at UT Health Northeast.

Professional Experience:

  • 1977-78 Intern, Internal Medicine, Temple University Hospital, Philadelphia, PA.
  • 1978-80 Resident, Internal Medicine, Temple University Hospital, Philadelphia, PA.
  • 1980 Board Certified, Internal Medicine, Am Board of Internal Medicine, No 77898.
  • 1980-83 Fellow, Pulmonary Disease Section, Temple University Hosp., Philadelphia, PA.
  • 1982 Board Certified Pulmonary Disease, Am. Board Int. Med. No. 77898.
  • 1984-88 Assistant/Associate Professor of Medicine, Temple University Health Science Center
    and UT Health Northeast (UT Health Northeast); Director, Medical ICUs.
  • 1988 Professor of Medicine and Chief, Pulmonary Division, The University of Texas Health Science
    Center at Tyler (UT Health Northeast).
  • 1996-03 Chairman, Department of Specialty Care Services, all medical specialties, UT Health Northeast.
  • 2003 Senior Vice President for Research, UT Health Northeast Currently serving in this capacity.
  • 2011 NIH SMARTT Review Panel.
  • 2012-13 Chair, NIH Translational PO-1 Review Panel.
  • 2013 Dean, School of Medical Biological Sciences, UT Health Northeast.
  • 2014 NIH VITA Advisory Board.

Research Interest:

Coagulation, Fibrinolysis, Regulation of Gene Expression, Acute and Chronic Lung Injury, Pleural Injury, Lung and Pleural Neoplasia.

Current Projects:

  • Control of the fibrin turnover in pleural disease.
  • Development of new therapeutics for lung and pleural fibrosis.

Current Grant Support:

  • NIH 1P50 HL 107186-01
    NIH/NHLBI - S. Idell (Contact); A. Komissarov (Co-PI)
    PAI-1 Targeted Intrapleural Fibrinolytic Therapy
    The primary goals of this project are to test various strategies that target plasminogen activator inhibitor-1 (PAI-1) in the preclinical treatment of pleural loculation. The objective of this work is to determine if PAI-1-targeted approaches confer advantages that are of potential clinical benefit over current pharmacologic approaches in anticipation of future clinical trial testing of PAI-1 targeted interventions that prove to be effective in our models of pleural injury.
  • NHLBI SMARTT Idell/Mazar (PI)
    scuPA for the Treatment of Complicated Parapneumonic Effusions
    The NHLBI Science Moving towArds Research Translation and Therapy program (SMARTT) contract facilitates the translation of novel discoveries into successful new therapies for heart, lung, and blood diseases. Support for cGMP manufacturing, GLP-compliant pharmacology/toxicology IND-enabling studies and regulatory support is provided for an IND submission for the zymogen form of urokinase, scuPA. (No specified end date).

Completed Research Support:

  • NIH 1R21HL097216-01A2
    NIH/NHLBI - Tang, H. (PI)
    PKD Family Kinase Function and Signaling in Lung Fibroblasts
    This project will test the hypothesis that PKD family kinases may play critical roles in lung fibroblast biology, including the fibroblast activation, proliferation, and the production of extracellular matrix, which may offer novel drugable targets for halting the progression of idiopathic pulmonary fibrosis.
  • NIH PO1 HL 076406-05
    NIH/NHLBI - Idell S. (PI)
    Fibrinolytic Pathways in Lung Injury and Repair
    This project will elucidate novel pathways by which the fibrinolytic system influences acute injury and repair in the lung and pleural compartment. There is no overlap with the present application.
  • NIH RAID 1 XO-1NS063898-01A1 - S. Idell (PI)
    IND-enabling toxicology, pharmacology and safety studies of recombinant scuPA for treatment for plueral loculation. This is a grant to perform toxicology studies on scuPA, a drug that will be prepared for clinical trial testing through work done as part of this grant. There is no overlap with the current project.
  • FAMRI Clinical Innovator Award - S. Shetty (PI)
    Control of PAI-1 in passive smoke exposure
    In these studies the role of PAI-1 in the control of lung epithelial cell viability and airway remodeling induced by passive smoke exposure in mice will be determined. There is no overlap with the studies proposed in this application.
  • NIH 1R21HL093547-01 - S. Shetty (PI)
    Regulation of lung epithelial injury by plasminogen activator inhibitor-1
    The primary goal of this project is to evaluate how p53-induced PAI-1 and inhibition of PAI-1 expression contributes to cellular adhesion to vitronectin, Akt phosphorylation, death receptor and mitochondrial pathways of apoptosis during airway and alveolar epithelial injury and to determine if p53-induced PAI-1 expression and its inhibition contribute to polymorphonuclear leukocyte (PMN) efferocytosis by macrophages during lung injury. No overlap with the studies proposed in this application. Role: Co-investigator.
  • FAMRI - Idell S (PI)
    PAI-1 and Airway Remodeling in Passive Smoke Exposure
    In this project, we evaluated the role of PAI-1 in control of proteolysis and lung remodeling induced by exposure of mice to passive smoke exposure.

Research Overview:

Extravascular fibrin deposition accompanies diverse types of tissue injury and neoplasia. In the setting of acute and chronic lung injury, the fibrin gel forms a transitional matrix that undergoes remodeling associated with invasion by inflammatory cells and fibroblasts. These cells express procoagulants and fibrinolysins that govern the transformation of the transitional fibrin gel into fibrotic tissue. A similar process accounts for the desmolastic response that surrounds various tumors, including lung cancers and malignant mesothelioma. Tumors also invade host tissues via remodeling of the transitional fibrin gel.

We have been, and remain interested in the elucidation of how pathways of fibrin deposition; coagulation and fibrinolysis influence the course of acute and chronic lung injuries. More recently, we have also studied the role of these processes in the pathogenesis of malignant mesothelioma. We are currently studying how expression of various fibrinolysins, procoagulants and their inhibitors are regulated at the posttranscriptional level and how these molecules influence cellular function via signaling mechanisms.

Selected Papers and Abstracts:
(Selected from a total of 142)

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