Naftali Kaminski MD

Boehringer Ingelheim Pharmaceuticals, Inc. Professor of Medicine (Pulmonary); Section Chief (7/1/13 - present)

Research Interests

Genomics; microRNAs; Non-coding RNAs; Biomarkers; Idiopathic Pulmonary Fibrosis and other Interstitial Lung Disease; Advanced Lung Disease; Personalized Medicine; Systems Biology; High-throughput technologies; Matrix Mtealloproteases

Current Projects

Basic mechanisms of pulmonary fibrosis and other chronic lung diseases

  • Understanding and identifying the genetic and molecular networks that determine the lung phenotype using high throughput genomic and proteomic technologies.
  • Role of miRNA in advanced lung disease (IPF, Emphysema).
  • Role of other non-coding RNAs (lincRNAs) in advanced lung disease
  • Epigenomics of chronic lung disease.
  • Using computational approaches to Integrate clinical, biological, genomic and proteomic data to identify new molecular phenotypes of disease.
  • Role of the microbiome in defining lung phenotypes in chronic lung disease

New molecular targets in Pulmonary Fibrosis

  • The role of developmental pathways in lung injury and repair.
  • The role and regulation of matrix metaloproteases (MMP7, MMP19) in human pulmonary fibrosis.
  • The role and regulation of microRNAs (let-7, mir-30, mir-154 families) in human pulmonary fibrosis
  • Downestream effect lincRNA perturbations in IPF
  • Using computational approaches to Integrate clinical, biological, genomic and proteomic data to identify new molecular phenotypes of disease.
  • Devlopment of microRNA mimics and inhibitors for therapy in lung fibrosis


Biomarker Discovery and Validation in chronic and progressive lung disease

  • Peripheral blood protein markers in lung fibrosis
  • Genetic predictors of outcome in lung fibrosis
  • Peripheral blood gene expression changes and disease progression
  • Can circulating microRNAs reflect organ phenotype and disease presence and prognosis

Research Summary

Dr Kaminski’s research is currently focused on improving our understanding and treatment of chronic lung diseases such as Idioathic Pulmonary Fibrosis (IPF), a chronic lung disease characterised by progressive scarring of the lungs, as well as COPD, Sarcoidosis and Asthma. His group applies cutting edge high throughput technologies that measure changes in the sequence, expression or regulation of all the genes in the human genome to identify the mechanisms, improve the diagnosis and develop new therapeutic targets.

Extensive Research Description

Advanced lung diseases affect a significant portion of the population, with the incidence of COPD/emphysema, asthma, and pulmonary fibrosis increasing annually. COPD is now the third leading cause of death in the US (www.cdc.gov). In 2003, 10.7 million U.S. adults were estimated to have COPD, although close to 24 million adults had evidence of abnormal lung function. The annual spending on COPD was approximately $37.2 billion in 2004, and that on asthma was estimated at $18 billion with millions of office and emergency room visits. In 2005, an estimated 1 in 20 deaths in the US were attributable to COPD (www.cdc.gov). Pulmonary fibrosis, although significantly less common, is also a substantial public health problem among the elderly. The incidence of idiopathic pulmonary fibrosis (IPF, the most severe form of pulmonary fibrosis) has doubled over the past decade and death rates continue to rise, especially among the elderly. While lung diseases have traditionally been defined by objective clinical characteristics, these characteristics usually do not predict outcome, response to therapy and morbidity and mortality. To realize the promise of personalized medicine, the current diagnostic approaches to chronic lung diseases should be modified to include both information on the genetics, epigenetics and microbiome of the individual and the diseased organ as well dynamic molecular information that can more precisely define the etiology, stage, and the biological activity of the disease process. Dr. Kaminski’s team main ambition is to uncover the mechanisms, and thus have a significant impact on the management of advanced lung diseases with a specific focus on IPF, a chronic progressive interstitial lung disease that is currently incurable. To study these mechanisms Dr. Kaminski’s team applies systems biology approaches that incorporate a combination of traditional molecular biology methods, high-throughput genomic technologies such as transcript level profiling (microarrays and next generation sequencing) of coding and non-coding RNA, genome scale analyses of gene variants, advanced bioinformatics approaches and targeted proteomic approaches. These studies have led to shifts in the perception of pulmonary fibrosis, the realization that aberrant activation of developmental pathways is at the core of lung fibrosis, the discovery of the role of microRNAs in IPF, the identification and validation of novel prognostic biomarkers in the bloodstream, as well many additional insights.


Selected Publications

  • MicroRNA mimicry blocks pulmonary fibrosis. Montgomery RL, Yu G, Latimer PA, Stack C, Robinson K, Dalby CM, Kaminski N, van Rooij E. EMBO Mol Med. 2014 Sep 19;6(10):1347-56. doi: 10.15252/emmm.201303604.
  • Matrix metalloproteinase-19 promotes metastatic behavior in vitro and is associated with increased mortality in non-small cell lung cancer. Yu G, Herazo-Maya JD, Nukui T, Romkes M, Parwani A, Juan-Guardela BM, Robertson J, Gauldie J, Siegfried JM, Kaminski N, Kass DJ. Am J Respir Crit Care Med. 2014 Oct 1;190(7):780-90. doi: 10.1164/rccm.201310-1903OC.

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