Skip to ContentSkip to Navigation
How to find us dr. C.A. (Corry-Anke) Brandsma

Research interests

Corry-Anke Brandsma, born in Leeuwarden in 1980, completed her master in Medical Biology at the RUG, Groningen in 2003. She was appointed as a PhD student from 2003-2007 on a joined project of the departments of Pathology and Pulmonary diseases of the UMCG on the inflammatory response in COPD. From 2007-2014 she worked as a post-doc on several research projects funded by the Dutch Lung Foundation. In 2011 she received international research fellowships from the European Respiratory Society and the Dutch Lung Foundation to work in the lab of Prof. J.C. Hogg in Vancouver (Canada). In 2014 she was appointed as staff member by the department of Pathology of the UMCG.

During her first post-doc, she focused on the role of adaptive immunity and B lymphocytes in COPD and demonstrated the presence of a smoke-induced specific immune response, which differed between COPD patients and healthy controls. After that, she steered her research focus to the role of accelerated lung aging and abnormal tissue repair in COPD, which is currently her main research focus. Using primary lung cells and lung tissue from well-characterized COPD patients and non-COPD control subjects she tries to unravel the molecular mechanisms underlying accelerated lung aging and abnormal tissue repair in COPD. For this, she uses a “multi-omics” approach combining information on changes in the genome (DNA), transcriptome (RNA, miRNA) and the proteome (protein) to identify causal molecular networks in COPD.  


COPD-derived fibroblasts secrete higher levels of senescence-associated secretory phenotype proteins

Current perspectives on the role of interleukin-1 signalling in the pathogenesis of asthma and COPD

Determinants of SARS-CoV-2 receptor gene expression in upper and lower airways

Epithelial-interleukin-1 inhibits collagen formation by airway fibroblasts: Implications for asthma

Genetic regulation of gene expression of MIF family members in lung tissue

Higher Secretion Levels of Senescence Associated Secretory Phenotype (SASP) Proteins by COPD-Derived Fibroblasts Compared to Control-Derived Fibroblasts

Identifying a nasal gene expression signature associated with hyperinflation and treatment response in severe COPD

IL-1 beta Induces a Pro-Inflammatory Fibroblast Micro-Environment That Impairs Alveolar Epithelial Organoid Formation

Integrated proteogenomic approach identifying a protein signature of COPD and a new splice variant of SORBS1

Link between increased cellular senescence and extracellular matrix changes in COPD

Read more


Interview Longwijzer