What is he best known for?
The fields of study he is best known for:
- Gene
- Internal medicine
- Inflammation
Nikolaos G. Frangogiannis focuses on Inflammation, Immunology, Myofibroblast, Fibrosis and Pathology.
His studies in Inflammation integrate themes in fields like Granulation tissue, Matrix metalloproteinase and Monocyte.
Nikolaos G. Frangogiannis interconnects Cancer research and Macrophage in the investigation of issues within Immunology.
His study in Myofibroblast is interdisciplinary in nature, drawing from both Wound healing, Fibroblast and Extracellular matrix, Cell biology.
The study incorporates disciplines such as Endocrinology, Transforming growth factor beta, Ventricular remodeling and Pathogenesis in addition to Fibrosis.
His Pathology research is multidisciplinary, incorporating elements of Mast cell, Ischemia and Infarction.
His most cited work include:
- The inflammatory response in myocardial infarction (1682 citations)
- The role of TGF-β Signaling in Myocardial Infarction and Cardiac Remodeling (686 citations)
- Regulation of the Inflammatory Response in Cardiac Repair (674 citations)
What are the main themes of his work throughout his whole career to date?
Inflammation, Internal medicine, Immunology, Fibrosis and Cell biology are his primary areas of study.
His work carried out in the field of Inflammation brings together such families of science as Cancer research, Angiogenesis, Cytokine and Pathology.
His Internal medicine research includes themes of Endocrinology and Cardiology.
Immunology is closely attributed to Macrophage in his research.
His Fibrosis research is multidisciplinary, incorporating perspectives in Cardiomyopathy and Transforming growth factor beta, Signal transduction, SMAD.
His Cell biology research incorporates themes from Fibroblast and Myofibroblast.
He most often published in these fields:
- Inflammation (41.05%)
- Internal medicine (33.62%)
- Immunology (31.88%)
What were the highlights of his more recent work (between 2018-2021)?
- Cell biology (24.45%)
- Inflammation (41.05%)
- Fibrosis (23.58%)
In recent papers he was focusing on the following fields of study:
The scientist’s investigation covers issues in Cell biology, Inflammation, Fibrosis, Cancer research and Myocardial infarction.
The Cell biology study combines topics in areas such as Phenotype, Fibroblast and Cell type.
His study in Inflammation is interdisciplinary in nature, drawing from both Cytokine and Heart failure.
His Cytokine study combines topics in areas such as Tumor necrosis factor alpha and Macrophage.
His studies examine the connections between Fibrosis and genetics, as well as such issues in Transforming growth factor, with regards to Cellular differentiation, Bone morphogenetic protein, Regeneration and Growth differentiation factor.
His work deals with themes such as Chemokine, CXCL10 and Growth factor, which intersect with Cancer research.
Between 2018 and 2021, his most popular works were:
- Cardiac fibrosis: Cell biological mechanisms, molecular pathways and therapeutic opportunities. (176 citations)
- The Extracellular Matrix in Ischemic and Nonischemic Heart Failure. (82 citations)
- Fibroblasts in the Infarcted, Remodeling, and Failing Heart (73 citations)
In his most recent research, the most cited papers focused on:
- Gene
- Internal medicine
- Inflammation
Nikolaos G. Frangogiannis spends much of his time researching Cell biology, Inflammation, Fibrosis, SMAD and Extracellular matrix.
His studies in Cell biology integrate themes in fields like Fibroblast and Infarction.
Inflammation is a subfield of Internal medicine that Nikolaos G. Frangogiannis studies.
His Fibrosis research is multidisciplinary, relying on both Macrophage, Transforming growth factor, Cell type and Cytokine.
As a part of the same scientific study, Nikolaos G. Frangogiannis usually deals with the Macrophage, concentrating on Cancer research and frequently concerns with Myocardial infarction.
Within one scientific family, he focuses on topics pertaining to Myofibroblast under SMAD, and may sometimes address concerns connected to Matrix, Matrix metalloproteinase, Gene knockdown, Coronary occlusion and Knockout mouse.
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