Harald Schmidt
Impact in
- Physiology top 0.02%
- Nitric Oxide and Endothelin Effects
- Biochemistry top 0.02%
- Eicosanoids and Hypertension Pharmacology
Papers in
- Physiology 160
- Nitric Oxide and Endothelin Effects 151
-
- Receptor Mechanisms and Signaling 24
- Co-authors
- Ulrich Walter (4 shared papers)Ulrich Förstermann (23 shared papers)Jennifer S. Pollock (16 shared papers)Ferid Murad (23 shared papers)Masaki Nakane (14 shared papers)Kirstin Wingler (19 shared papers)Timothy D. Warner (12 shared papers)Suzanne M. Lohmann (2 shared papers)
- Journals
- Free Radical Biology and Medicine (11 papers)Antioxidants and Redox Signaling (9 papers)Molecular Pharmacology (8 papers)Biochemical Journal (8 papers)Proceedings of the National Academy of Sciences (8 papers)
- Partner nations
- GermanyUnited StatesNetherlands
In The Last Decade
Harald Schmidt
350 papers receiving 28.2k citations
Harald Schmidt's Hit Papers
Peers
Comparison fields: 5 of 193
- Physiology 12.9k
- Biochemistry 2.9k
- Endocrine and Autonomic Systems 2.1k
- Neurology 1.6k
- Immunology 3.9k
Countries citing papers authored by Harald Schmidt
This map shows the geographic impact of Harald Schmidt'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 Harald Schmidt with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Harald Schmidt more than expected).
Fields of papers citing papers by Harald Schmidt
This network shows the impact of papers produced by Harald Schmidt. 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 Harald Schmidt. The network helps show where Harald Schmidt may publish in the future.
Co-authors
The 25 scholars most cited alongside Harald Schmidt, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.
All Works
Showing the 20 most-cited of 366 papers — load more, or switch the sort, to bring in the rest.
| # | Work | ||
|---|---|---|---|
| 1 | NO at work Hit paper breakdown → | 1994 | 1301 |
| 2 | Purification and characterization of particulate endothelium-derived relaxing factor synthase from cultured and native bovine aortic endothelial cells. Hit paper breakdown → | 1991 | 817 |
| 3 | Network pharmacology: curing causal mechanisms instead of treating symptoms Hit paper breakdown → | 2021 | 723 |
| 4 | Isoforms of nitric oxide synthase Characterization and purification from different cell types Hit paper breakdown → | 1991 | 717 |
| 5 | Clinical Relevance of Biomarkers of Oxidative Stress Hit paper breakdown → | 2015 | 672 |
| 6 | The nitric oxide and cGMP signal transduction system: regulation and mechanism of action Hit paper breakdown → | 1993 | 639 |
| 7 | Apocynin Is Not an Inhibitor of Vascular NADPH Oxidases but an Antioxidant Hit paper breakdown → | 2007 | 638 |
| 8 | NO-independent stimulators and activators of soluble guanylate cyclase: discovery and therapeutic potential Hit paper breakdown → | 2006 | 573 |
| 9 | Mapping of neural nitric oxide synthase in the rat suggests frequent co-localization with NADPH diaphorase but not with soluble guanylyl cyclase, and novel paraneural functions for nitrinergic signal transduction. Hit paper breakdown → | 1992 | 548 |
| 10 | Transcription Factor NRF2 as a Therapeutic Target for Chronic Diseases: A Systems Medicine Approach Hit paper breakdown → | 2018 | 516 |
| 11 | Calmodulin-dependent endothelium-derived relaxing factor/nitric oxide synthase activity is present in the particulate and cytosolic fractions of bovine aortic endothelial cells. Hit paper breakdown → | 1991 | 498 |
| 12 | 2004 | 455 | |
| 13 | 2014 | 449 | |
| 14 | Cloned human brain nitric oxide synthase is highly expressed in skeletal muscle Hit paper breakdown → | 1993 | 446 |
| 15 | 1992 | 434 | |
| 16 | 2006 | 370 | |
| 17 | 1992 | 352 | |
| 18 | 2005 | 347 | |
| 19 | 2013 | 323 | |
| 20 | 2008 | 323 |
About Harald Schmidt
Harald Schmidt is a scholar working on Physiology, Molecular Biology, Immunology, Cardiology and Cardiovascular Medicine and Biochemistry, having authored 366 papers that have together received 29.0k indexed citations. Recurring topics across this work include Nitric Oxide and Endothelin Effects (151 papers), Neutrophil, Myeloperoxidase and Oxidative Mechanisms (47 papers), Eicosanoids and Hypertension Pharmacology (35 papers), Renin-Angiotensin System Studies (30 papers), Receptor Mechanisms and Signaling (24 papers), Neuroscience and Neuropharmacology Research (21 papers), Neuroscience of respiration and sleep (18 papers) and Neuropeptides and Animal Physiology (15 papers). The work is most often cited by research in Physiology (12.9k citations), Biochemistry (2.9k citations), Endocrine and Autonomic Systems (2.1k citations), Neurology (1.6k citations) and Immunology (3.9k citations). Harald Schmidt has collaborated with scholars based in Germany, United States and Netherlands. Frequent co-authors include Ulrich Walter, Ulrich Förstermann, Jennifer S. Pollock, Ferid Murad, Masaki Nakane, Kirstin Wingler, Timothy D. Warner, Suzanne M. Lohmann, Jane A. Mitchell and Richard J. Weinberg. Their work appears in journals such as Free Radical Biology and Medicine, Antioxidants and Redox Signaling, Molecular Pharmacology, Biochemical Journal and Proceedings of the National Academy of Sciences.
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.