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Researcher · Instytut Biologii Doświadczalnej im. Marcelego Nenckiego · Poland

Mariusz Roman Wieckowski

Mariusz Roman Wieckowski publishes mostly in Molecular Biology, Epidemiology and Clinical Biochemistry, on topics such as Mitochondrial Function and Pathology, ATP Synthase and ATPases Research and Metabolism and Genetic Disorders.

ORCID 0000-0003-0789-4521 OpenAlex
World rank
#55,414
of 7,710,434 ranked researchers
Rank in Poland
#452
of 100,960
Works
228
Citations
21k
Citations per work
90.4
h-index
70
i10-index 155Top 1.1% in Molecular Biology
Mariusz Roman Wieckowski

What does Mariusz Roman Wieckowski research?

Mariusz Roman Wieckowski's work is mostly in Biochemistry, Genetics and Molecular Biology (51%), Medicine (14%).

Life Sciences: 116 works · 50.7% of their workBiochemistry, Genetics and Molecular Biology: 116 works · 50.7% of their workMolecular Biology: 95 works · 41.6% of their workClinical Biochemistry: 12 works · 5.3% of their workCell Biology: 9 works · 3.8% of their workEverything else: 80 works · 35.3% of their workHealth Sciences: 32 works · 14.0% of their workMedicine: 32 works · 14.0% of their workEpidemiology: 16 works · 6.9% of their workPhysiology: 10 works · 4.5% of their workPathology and Forensic Medicine: 6 works · 2.6% of their workTHEIR WORKMariusz RomanWieckowski228works
Life Sciences51%Health Sciences14%

Their six largest subfields, inside their fields and domains; the grey slice is everything else they publish. The interactive view splits every one of their works down to single topics.

The fields and subfields, with their numbers
    1. Biochemistry, Genetics and Molecular Biology11650.7%
  2. Everything else8035.3%
    1. Medicine3214.0%
  1. 1Molecular Biology42% of their works
  2. 2Epidemiology7% of their works
  3. 3Clinical Biochemistry5% of their works
  4. 4Physiology4% of their works
  5. 5Cell Biology4% of their works
  6. 6Pathology and Forensic Medicine3% of their works

Research topics

Which keywords describe Mariusz Roman Wieckowski's research?

The keywords of their largest research topics: Cell Death, Metabolic Regulation, Mitochondrial Dysfunction, Oxidative Stress, Mitochondria, Reactive Oxygen Species, Mitochondrial Fission and Mitochondrial Fusion.

Size is their works in the topics tagged with each word, from their 8 largest topics. Each links to the topic it comes from most. The words come from the keyword list OpenAlex gives each topic, not from the text of the papers, so a word can appear that none of the papers uses.

All 24 words, with their numbers
  1. Cell Death1533 topics
  2. Metabolic Regulation1442 topics
  3. Mitochondrial Dysfunction1442 topics
  4. Oxidative Stress1422 topics
  5. Mitochondria1322 topics
  6. Reactive Oxygen Species1322 topics
  7. Mitochondrial Fission1211 topic
  8. Mitochondrial Fusion1211 topic
  9. Apoptosis593 topics
  10. ATP Synthase491 topic
  11. Vacuolar ATPases491 topic
  12. Insulin Resistance362 topics
  13. Biochemical Genetics321 topic
  14. Metabolic Disorders321 topic
  15. Autophagy271 topic
  16. Disease271 topic
  17. Brown Adipose Tissue231 topic
  18. Thermogenesis231 topic
  19. Endoplasmic Reticulum211 topic
  20. Stress211 topic
  21. NAFLD131 topic
  22. NASH131 topic
  23. Bcl-2 Family111 topic
  24. TNF Signaling111 topic

Where does Mariusz Roman Wieckowski work?

Mariusz Roman Wieckowski's main affiliation in the publication record is Instytut Biologii Doświadczalnej im. Marcelego Nenckiego, Poland.

How many publications and citations does Mariusz Roman Wieckowski have?

OpenAlex counts 228 works and 20,613 citations for Mariusz Roman Wieckowski, an h-index of 70, ranking #55,414 of 7,710,434 researchers worldwide on the quality score.

Ranked on field-normalised citation excellence (50%), output (30%) and citations (20%). Counts come from OpenAlex author records, which occasionally merge different people who share a name or split one person into several.

Papers, co-authors, who cited this work and researchers on the nearest topics have tabs of their own, above. Is this your page? Claim it with your ORCID iD, or request a correction or removal.

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