What is he best known for?
The fields of study he is best known for:
- Gene
- Internal medicine
- DNA
His primary areas of study are Cell biology, Inflammation, Internal medicine, Endocrinology and Adipose tissue.
His Cell biology research is multidisciplinary, relying on both Cancer research, Cellular differentiation, Transcription factor, Regulation of gene expression and Adipogenesis.
His Cellular differentiation research integrates issues from Molecular biology and Neointima.
His Inflammation research includes elements of Adipokine, Cell adhesion molecule and Pathology.
Adipose tissue macrophages is the focus of his Adipose tissue research.
His studies deal with areas such as 3T3-L1, Adipocyte, Immune system, Adoptive cell transfer and Cell type as well as Adipose tissue macrophages.
His most cited work include:
- CD8 + effector T cells contribute to macrophage recruitment and adipose tissue inflammation in obesity (1528 citations)
- Overexpression of Monocyte Chemoattractant Protein-1 in Adipose Tissues Causes Macrophage Recruitment and Insulin Resistance (702 citations)
- RNA-Methylation-Dependent RNA Processing Controls the Speed of the Circadian Clock (498 citations)
What are the main themes of his work throughout his whole career to date?
Ichiro Manabe mostly deals with Cell biology, Internal medicine, Endocrinology, Inflammation and Transcription factor.
Ichiro Manabe interconnects Fibrosis, Neointima and Vascular smooth muscle, Smooth muscle in the investigation of issues within Cell biology.
His Internal medicine study often links to related topics such as Cardiology.
His study of Angiotensin II is a part of Endocrinology.
His research in Inflammation intersects with topics in Adipose tissue, Macrophage, Immune system and Pathology.
The Adipose tissue study combines topics in areas such as Stromal cell and Obesity.
He most often published in these fields:
- Cell biology (35.05%)
- Internal medicine (26.69%)
- Endocrinology (18.01%)
What were the highlights of his more recent work (between 2015-2021)?
- Cell biology (35.05%)
- Inflammation (17.68%)
- Macrophage (5.79%)
In recent papers he was focusing on the following fields of study:
Cell biology, Inflammation, Macrophage, Internal medicine and Immunology are his primary areas of study.
His Cell biology research is multidisciplinary, incorporating perspectives in Fibrosis and Cholesterol, Foam cell, Lipoprotein.
His Inflammation research incorporates themes from Cancer, Immune system, Function, Disease and Extracellular matrix.
His study in Immune system is interdisciplinary in nature, drawing from both Adipose tissue, Lipid metabolism, Proinflammatory cytokine and Regulator.
Ichiro Manabe has researched Internal medicine in several fields, including Endocrinology and Cardiology.
His Immunology study combines topics from a wide range of disciplines, such as Lymphedema and Homeostasis.
Between 2015 and 2021, his most popular works were:
- HIF-1α-PDK1 axis-induced active glycolysis plays an essential role in macrophage migratory capacity (115 citations)
- SREBP1 Contributes to Resolution of Pro-inflammatory TLR4 Signaling by Reprogramming Fatty Acid Metabolism (111 citations)
- Obesity accelerates T cell senescence in murine visceral adipose tissue (102 citations)
In his most recent research, the most cited papers focused on:
- Gene
- Internal medicine
- DNA
His main research concerns Inflammation, Cell biology, Immunology, Molecular biology and Internal medicine.
His biological study spans a wide range of topics, including Regulation of gene expression, Macrophage, Immune system and Fatty acid metabolism.
The study incorporates disciplines such as Diabetes mellitus, Cancer, Adipose tissue and Disease in addition to Immune system.
His Cell biology research incorporates elements of Fibrosis, Glycolysis, PER2 and Circadian rhythm.
His Immunology research includes themes of Vascular endothelial growth factor C, Lymphedema, Edema and Lymphangiogenesis.
His Internal medicine study integrates concerns from other disciplines, such as Endocrinology and Adoptive cell transfer.
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