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NYU Langone Provider

Matthias C. Kugler, MD

NYU Langone Provider
  • Specialties: Pulmonary Medicine, Critical Care
  • Treats: Adults
  • Languages: English, German
  • Phone: 212-598-6351
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Board Certifications
  • American Board of Internal Medicine (Critical Care Medicine), 2012
  • American Board of Internal Medicine (Pulmonary Disease), 2011
  • American Board of Internal Medicine - Internal Medicine, 2009
Education and Training
  • Fellowship, NYU School of Medicine, Pulmonary and Critical Care Medicine, 2012
  • Residency, NYU School of Medicine, Internal Medicine, 2009
  • MD from Technical University of Munich, 2003

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This provider accepts the following insurance plans.

  • Aetna
    • Aetna HMO
    • Aetna Indemnity
    • Aetna Medicare
    • Aetna POS
    • Aetna PPO/EPO
  • Agewell
    • Agewell
  • Cigna
    • Cigna EPO/POS
    • Cigna PPO
  • ElderPlan
    • ElderPlan
  • Emblem
    • Emblem Select Care Exchange
  • Empire Blue Cross Blue Shield
    • Empire Blue Cross Blue Shield EPO
    • Empire Blue Cross Blue Shield HMO
    • Empire Blue Cross Blue Shield HealthPlus
    • Empire Blue Cross Blue Shield HealthPlus Essential
    • Empire Blue Cross Blue Shield Indemnity
    • Empire Blue Cross Blue Shield MediBlue
    • Empire Blue Cross Blue Shield POS
    • Empire Blue Cross Blue Shield PPO
  • GHI
    • GHI CBP
    • GHI HMO
  • HIP
    • HIP Access I
    • HIP Access II
    • HIP Child Health
    • HIP Essential
    • HIP HMO
    • HIP Medicaid
    • HIP Medicare
    • HIP POS
  • HealthSmart
    • HealthSmart (WTC)
View All Accepted Plans This list of insurances changes regularly, and insurance plans listed may not be accepted at all office locations for this provider. Before your appointment, please confirm with your insurance company that this provider accepts your insurance.

Locations and Appointments

NYU Langone Orthopedic Pulmonary Associates

301 East 17th Street, Suite 550, New York, NY 10003






adult fibrosing lung diseases, idiopathic pulmonary fibrosis, IPF

Research Summary

Two areas of interest evolved from my research and clinical activities. On the cell biology level, I am interested in how cell surface receptors communicate with their environment in physiologic and pathophysiologic states. The functional consequences of altered signaling are of particular interest for me as a physician since they give me further insight into disease mechanisms, such as aberrant integrin or growth factor receptor signaling in pulmonary fibrosis. On the clinical level, I have become particularly interested in IPF (idiopathic pulmonary fibrosis), a fatal, progressive lung disease with unpredictable clinical course, a median survival of <4 years and no effective treatment. Despite extensive research its underlying mechanisms remain unclear. One potential way I have studied involves EMT. In EMT, epithelial cell injury induces phenotype change to a mesenchymal type, resulting in interstitial matrix accumulation in alveolar walls and progressive pulmonary fibrosis with loss of function. Another potential mechanism I am currently studying involves embryonic signaling pathways, such as Hedgehog (HH) signaling, which are usually suppressed in adult uninjured lung, but might become reactivated as pathogenic mechanism in IPF.

In our lab we have shown HH pathway reactivation in lung fibroblasts in two important settings: (1) during alveolar septum formation in the postnatal lung and (2) in bleomycin-injured fibrotic lung. In the early postnatal developmental setting, inhibition of HH signaling produced alveolar airspace enlargement and septum wall thinning without affecting septum formation. This indicates the importance of precise temporal decrease in mesenchyme for normal lung structure. In the pathophysiological setting, the exacerbation of bleomycin-induced fibrosis by SHH over-expression implies that aberrant pathway activity prevents the demise of lung fibroblasts during fibrosis resolution.

The long-term goals of my work are to better understand the molecular signatures of pulmonary fibrosis by studying their characteristics in pathophysiologically relevant mouse models to elucidate novel mechanisms and improve treatment options.

These focus areas and their associated publications are derived from PubMed and the MeSH term library. *
represents one publication
*Due to PubMed processing times, the most recent publications may not be reflected in the timeline.

Read All Publications (24)