Carmen Veith

2.3k total citations · 1 hit paper
15 papers, 1.5k citations indexed

About

Carmen Veith is a scholar working on Molecular Biology, Pulmonary and Respiratory Medicine and Physiology. According to data from OpenAlex, Carmen Veith has authored 15 papers receiving a total of 1.5k indexed citations (citations by other indexed papers that have themselves been cited), including 6 papers in Molecular Biology, 5 papers in Pulmonary and Respiratory Medicine and 5 papers in Physiology. Recurrent topics in Carmen Veith's work include Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis (5 papers), Genomics, phytochemicals, and oxidative stress (3 papers) and SARS-CoV-2 and COVID-19 Research (2 papers). Carmen Veith is often cited by papers focused on Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis (5 papers), Genomics, phytochemicals, and oxidative stress (3 papers) and SARS-CoV-2 and COVID-19 Research (2 papers). Carmen Veith collaborates with scholars based in Netherlands, United States and Germany. Carmen Veith's co-authors include Agnes W. Boots, Nicolas Kahn, Marc A. Schneider, Michael Kreuter, Michael Meister, H. Winter, Christian Conrad, Thomas Muley, Robert Lorenz Chua and Roland Eils and has published in prestigious journals such as Nature Communications, The EMBO Journal and Journal of Allergy and Clinical Immunology.

In The Last Decade

Carmen Veith

15 papers receiving 1.5k citations

Hit Papers

SARS ‐CoV‐2 receptor ACE 2 and TMPRSS 2 are primarily exp... 2020 2026 2022 2024 2020 200 400 600

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name h Career Trend Papers Cites
Carmen Veith Netherlands 13 732 395 264 239 215 15 1.5k
Kevin Godbout United States 6 1.1k 1.6× 809 2.0× 244 0.9× 135 0.6× 331 1.5× 7 3.6k
Mary Donoghue United States 5 919 1.3× 664 1.7× 143 0.5× 100 0.4× 277 1.3× 5 2.9k
Michael Gosselin United States 6 902 1.2× 681 1.7× 563 2.1× 114 0.5× 273 1.3× 9 3.2k
Jakub Rosik Poland 15 324 0.4× 445 1.1× 110 0.4× 147 0.6× 161 0.7× 34 1.3k
Donghong Yang China 16 558 0.8× 397 1.0× 105 0.4× 282 1.2× 258 1.2× 51 1.4k
Filip Machaj Poland 14 301 0.4× 433 1.1× 100 0.4× 134 0.6× 153 0.7× 25 1.2k
Zhonglin Chai Australia 20 441 0.6× 365 0.9× 88 0.3× 92 0.4× 205 1.0× 52 1.6k
Yunjiao Zhou China 15 573 0.8× 390 1.0× 102 0.4× 93 0.4× 223 1.0× 27 1.3k
Kai Meng China 21 341 0.5× 510 1.3× 421 1.6× 75 0.3× 209 1.0× 65 1.6k

Countries citing papers authored by Carmen Veith

Since Specialization
Citations

This map shows the geographic impact of Carmen Veith's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Carmen Veith with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Carmen Veith more than expected).

Fields of papers citing papers by Carmen Veith

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Carmen Veith. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Carmen Veith. The network helps show where Carmen Veith may publish in the future.

Co-authorship network of co-authors of Carmen Veith

This figure shows the co-authorship network connecting the top 25 collaborators of Carmen Veith. A scholar is included among the top collaborators of Carmen Veith based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Carmen Veith. Carmen Veith is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

15 of 15 papers shown
1.
Veith, Carmen, Marc A. Schneider, Albert van der Vliet, et al.. (2023). Differences in Treatment Response in Bronchial Epithelial Cells from Idiopathic Pulmonary Fibrosis (IPF) Patients: A First Step towards Personalized Medicine?. Antioxidants. 12(2). 443–443. 1 indexed citations
2.
Talwar, Deepti, Colin G. Miller, Łukasz Szyrwiel, et al.. (2023). The GAPDH redox switch safeguards reductive capacity and enables survival of stressed tumour cells. Nature Metabolism. 5(4). 660–676. 59 indexed citations
3.
Lukassen, Soeren, Robert Lorenz Chua, Timo B. Trefzer, et al.. (2020). SARS-CoV-2 receptor ACE2 and TMPRSS2 are primarily expressed in bronchial transient secretory cells. The EMBO Journal. e105114–e105114. 253 indexed citations
4.
Lukassen, Soeren, Robert Lorenz Chua, Timo B. Trefzer, et al.. (2020). SARS ‐CoV‐2 receptor ACE 2 and TMPRSS 2 are primarily expressed in bronchial transient secretory cells. The EMBO Journal. 39(10). e105114–e105114. 703 indexed citations breakdown →
5.
Boots, Agnes W., Carmen Veith, Catrin Albrecht, et al.. (2020). The dietary antioxidant quercetin reduces hallmarks of bleomycin-induced lung fibrogenesis in mice. BMC Pulmonary Medicine. 20(1). 112–112. 45 indexed citations
6.
Boots, Agnes W., Carmen Veith, Michael Kreuter, et al.. (2020). Towards personalized medicine in idiopathic pulmonary fibrosis by screening exhaled volatiles in patients’ primary bronchial epithelial cells. 605–605. 1 indexed citations
7.
Veith, Carmen, Milena Hristova, Karamatullah Danyal, et al.. (2020). Profibrotic epithelial TGF-β1 signaling involves NOX4-mitochondria cross talk and redox-mediated activation of the tyrosine kinase FYN. American Journal of Physiology-Lung Cellular and Molecular Physiology. 320(3). L356–L367. 18 indexed citations
8.
Veith, Carmen, et al.. (2019). Redox Imbalance in Idiopathic Pulmonary Fibrosis: A Role for Oxidant Cross-Talk Between NADPH Oxidase Enzymes and Mitochondria. Antioxidants and Redox Signaling. 31(14). 1092–1115. 75 indexed citations
9.
Heppner, David E., Christopher M. Dustin, Chenyi Liao, et al.. (2018). Direct cysteine sulfenylation drives activation of the Src kinase. Nature Communications. 9(1). 4522–4522. 97 indexed citations
10.
Shi, Quan, Agnes W. Boots, L.M. Maas, et al.. (2017). Effect of interleukin (IL)-8 on benzo[a]pyrene metabolism and DNA damage in human lung epithelial cells. Toxicology. 381. 64–74. 14 indexed citations
11.
Veith, Carmen, Marjolein Drent, Aalt Bast, Frederik‐Jan van Schooten, & Agnes W. Boots. (2017). The disturbed redox-balance in pulmonary fibrosis is modulated by the plant flavonoid quercetin. Toxicology and Applied Pharmacology. 336. 40–48. 80 indexed citations
12.
Shi, Quan, L.M. Maas, Carmen Veith, Frederik‐Jan van Schooten, & Roger Godschalk. (2016). Acidic cellular microenvironment modifies carcinogen-induced DNA damage and repair. Archives of Toxicology. 91(6). 2425–2441. 30 indexed citations
13.
Hristova, Milena, Aida Habibovic, Carmen Veith, et al.. (2015). Airway epithelial dual oxidase 1 mediates allergen-induced IL-33 secretion and activation of type 2 immune responses. Journal of Allergy and Clinical Immunology. 137(5). 1545–1556.e11. 115 indexed citations
14.
Shi, Quan, Guido R.M.M. Haenen, L.M. Maas, et al.. (2015). Inflammation-associated extracellular β-glucuronidase alters cellular responses to the chemical carcinogen benzo[a]pyrene. Archives of Toxicology. 90(9). 2261–2273. 25 indexed citations
15.
Hristova, Milena, Carmen Veith, Aida Habibovic, et al.. (2014). Identification of DUOX1-dependent redox signaling through protein S-glutathionylation in airway epithelial cells. Redox Biology. 2. 436–446. 25 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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