LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 227

Search options

  1. Article: Macrophages, apoptotic cells and cholesterol -- strategies for survival: an interview with Dr. Ira Tabas. Interview by Helene F. Rosenberg.

    Tabas, Ira

    Journal of leukocyte biology

    2007  Volume 82, Issue 5, Page(s) 1051–1052

    MeSH term(s) Acetyl-CoA C-Acetyltransferase/genetics ; Acetyl-CoA C-Acetyltransferase/physiology ; Animals ; Apoptosis/physiology ; Cell Communication ; Cholesterol/physiology ; Humans ; Macrophages, Peritoneal/cytology ; Macrophages, Peritoneal/metabolism ; Phagocytes/cytology ; Phagocytes/metabolism ; Phagocytosis
    Chemical Substances Cholesterol (97C5T2UQ7J) ; Acat1 protein, mouse (EC 2.3.1.9) ; Acetyl-CoA C-Acetyltransferase (EC 2.3.1.9)
    Language English
    Publishing date 2007-11
    Publishing country United States
    Document type Interview ; Portraits
    ZDB-ID 605722-6
    ISSN 1938-3673 ; 0741-5400
    ISSN (online) 1938-3673
    ISSN 0741-5400
    DOI 10.1189/jlb.1307192
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  2. Article ; Online: Efferocytosis-induced lactate enables the proliferation of pro-resolving macrophages to mediate tissue repair.

    Ngai, David / Schilperoort, Maaike / Tabas, Ira

    Nature metabolism

    2023  Volume 5, Issue 12, Page(s) 2206–2219

    Abstract: The clearance of apoptotic cells by macrophages (efferocytosis) prevents necrosis and inflammation and activates pro-resolving pathways, including continual efferocytosis. A key resolution process in vivo is efferocytosis-induced macrophage proliferation ...

    Abstract The clearance of apoptotic cells by macrophages (efferocytosis) prevents necrosis and inflammation and activates pro-resolving pathways, including continual efferocytosis. A key resolution process in vivo is efferocytosis-induced macrophage proliferation (EIMP), in which apoptotic cell-derived nucleotides trigger Myc-mediated proliferation of pro-resolving macrophages. Here we show that EIMP requires a second input that is integrated with cellular metabolism, notably efferocytosis-induced lactate production. Lactate signalling via GPR132 promotes Myc protein stabilization and subsequent macrophage proliferation. This mechanism is validated in vivo using a mouse model of dexamethasone-induced thymocyte apoptosis, which elevates apoptotic cell burden and requires efferocytosis to prevent inflammation and necrosis. Thus, EIMP, a key process in tissue resolution, requires inputs from two independent processes: a signalling pathway induced by apoptotic cell-derived nucleotides and a cellular metabolism pathway involving lactate production. These findings illustrate how seemingly distinct pathways in efferocytosing macrophages are integrated to carry out a key process in tissue resolution.
    MeSH term(s) Humans ; Phagocytosis ; Efferocytosis ; Lactic Acid/metabolism ; Macrophages/metabolism ; Inflammation/metabolism ; Necrosis/metabolism ; Nucleotides/metabolism ; Cell Proliferation
    Chemical Substances Lactic Acid (33X04XA5AT) ; ethyl isopropyl methylphosphonate ; Nucleotides
    Language English
    Publishing date 2023-11-27
    Publishing country Germany
    Document type Journal Article
    ISSN 2522-5812
    ISSN (online) 2522-5812
    DOI 10.1038/s42255-023-00921-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  3. Article ; Online: Heart disease: Death-defying plaque cells.

    Tabas, Ira

    Nature

    2016  Volume 536, Issue 7614, Page(s) 32–33

    MeSH term(s) Cell Death ; Coronary Artery Disease ; Death, Sudden, Cardiac ; Heart Diseases ; Humans ; Plaque, Amyloid
    Language English
    Publishing date 2016--04
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/nature18916
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  4. Article ; Online: Efferocytosis in liver disease.

    Shi, Hongxue / Moore, Mary P / Wang, Xiaobo / Tabas, Ira

    JHEP reports : innovation in hepatology

    2023  Volume 6, Issue 1, Page(s) 100960

    Abstract: The process of dead cell clearance by phagocytic cells, called efferocytosis, prevents inflammatory cell necrosis and promotes resolution and repair. Defective efferocytosis contributes to the progression of numerous diseases in which cell death is ... ...

    Abstract The process of dead cell clearance by phagocytic cells, called efferocytosis, prevents inflammatory cell necrosis and promotes resolution and repair. Defective efferocytosis contributes to the progression of numerous diseases in which cell death is prominent, including liver disease. Many gaps remain in our understanding of how hepatic macrophages carry out efferocytosis and how this process goes awry in various types of liver diseases. Thus far, studies have suggested that, upon liver injury, liver-resident Kupffer cells and infiltrating monocyte-derived macrophages clear dead cells, limit inflammation, and, through macrophage reprogramming, repair liver damage. However, in unusual settings, efferocytosis can promote liver disease. In this review, we will focus on efferocytosis in various types of acute and chronic liver diseases, including metabolic dysfunction-associated steatohepatitis. Understanding the mechanisms and consequences of efferocytosis by hepatic macrophages has the potential to shed new light on liver disease pathophysiology and to guide new treatment strategies to prevent disease progression.
    Language English
    Publishing date 2023-11-16
    Publishing country Netherlands
    Document type Journal Article ; Review
    ISSN 2589-5559
    ISSN (online) 2589-5559
    DOI 10.1016/j.jhepr.2023.100960
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  5. Article ; Online: 2016 Russell Ross Memorial Lecture in Vascular Biology: Molecular-Cellular Mechanisms in the Progression of Atherosclerosis.

    Tabas, Ira

    Arteriosclerosis, thrombosis, and vascular biology

    2016  Volume 37, Issue 2, Page(s) 183–189

    Abstract: Atherosclerosis is initiated by the subendothelial accumulation of apoB-lipoproteins, which initiates a sterile inflammatory response dominated by monocyte-macrophages but including all classes of innate and adaptive immune cells. These inflammatory ... ...

    Abstract Atherosclerosis is initiated by the subendothelial accumulation of apoB-lipoproteins, which initiates a sterile inflammatory response dominated by monocyte-macrophages but including all classes of innate and adaptive immune cells. These inflammatory cells, together with proliferating smooth muscle cells and extracellular matrix, promote the formation of subendothelial lesions or plaques. In the vast majority of cases, these lesions do not cause serious clinical symptoms, which is due in part to a resolution-repair response that limits tissue damage. However, a deadly minority of lesions progress to the point where they can trigger acute lumenal thrombosis, which may then cause unstable angina, myocardial infarction, sudden cardiac death, or stroke. Many of these clinically dangerous lesions have hallmarks of defective inflammation resolution, including defective clearance of dead cells (efferocytosis), necrosis, a defective scar response, and decreased levels of lipid mediators of the resolution response. Efferocytosis is both an effector arm of the resolution response and an inducer of resolution mediators, and thus its defect in advanced atherosclerosis amplifies plaque progression. Preclinical causation/treatment studies have demonstrated that replacement therapy with exogenously administered resolving mediators can improve lesional efferocytosis and prevent plaque progression. Work in this area has the potential to potentiate the cardiovascular benefits of apoB-lipoprotein-lowering therapy.
    MeSH term(s) Animals ; Apolipoproteins B/metabolism ; Apoptosis ; Arteries/immunology ; Arteries/metabolism ; Arteries/pathology ; Atherosclerosis/immunology ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Atherosclerosis/therapy ; Disease Progression ; Humans ; Inflammation/immunology ; Inflammation/metabolism ; Inflammation/pathology ; Inflammation/therapy ; Inflammation Mediators/metabolism ; Necrosis ; Plaque, Atherosclerotic ; Prognosis ; Signal Transduction
    Chemical Substances Apolipoproteins B ; Inflammation Mediators
    Language English
    Publishing date 2016-12-15
    Publishing country United States
    Document type Journal Article ; Lecture ; Review
    ZDB-ID 1221433-4
    ISSN 1524-4636 ; 1079-5642
    ISSN (online) 1524-4636
    ISSN 1079-5642
    DOI 10.1161/ATVBAHA.116.308036
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  6. Article ; Online: Intracellular and Intercellular Aspects of Macrophage Immunometabolism in Atherosclerosis.

    Tabas, Ira / Bornfeldt, Karin E

    Circulation research

    2020  Volume 126, Issue 9, Page(s) 1209–1227

    Abstract: Macrophage immunometabolism, the changes in intracellular metabolic pathways that alter the function of these highly plastic cells, has been the subject of intense interest in the past few years, in part because macrophage immunometabolism plays ... ...

    Abstract Macrophage immunometabolism, the changes in intracellular metabolic pathways that alter the function of these highly plastic cells, has been the subject of intense interest in the past few years, in part because macrophage immunometabolism plays important roles in atherosclerosis and other inflammatory diseases. In this review article, part of the
    MeSH term(s) Animals ; Arteries/immunology ; Arteries/metabolism ; Arteries/pathology ; Atherosclerosis/immunology ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Energy Metabolism ; Humans ; Macrophages/immunology ; Macrophages/metabolism ; Macrophages/pathology ; Plaque, Atherosclerotic ; Signal Transduction
    Language English
    Publishing date 2020-04-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.119.315939
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  7. Article ; Online: Making things stick in the fight against atherosclerosis.

    Tabas, Ira

    Circulation research

    2013  Volume 112, Issue 8, Page(s) 1094–1096

    Language English
    Publishing date 2013-04-10
    Publishing country United States
    Document type Comment ; Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.113.301227
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  8. Article ; Online: The role of efferocytosis-fueled macrophage metabolism in the resolution of inflammation.

    Schilperoort, Maaike / Ngai, David / Sukka, Santosh R / Avrampou, Kleopatra / Shi, Hongxue / Tabas, Ira

    Immunological reviews

    2023  Volume 319, Issue 1, Page(s) 65–80

    Abstract: The phagocytosis of dying cells by macrophages, termed efferocytosis, is a tightly regulated process that involves the sensing, binding, engulfment, and digestion of apoptotic cells. Efferocytosis not only prevents tissue necrosis and inflammation caused ...

    Abstract The phagocytosis of dying cells by macrophages, termed efferocytosis, is a tightly regulated process that involves the sensing, binding, engulfment, and digestion of apoptotic cells. Efferocytosis not only prevents tissue necrosis and inflammation caused by secondary necrosis of dying cells, but it also promotes pro-resolving signaling in macrophages, which is essential for tissue resolution and repair following injury or inflammation. An important factor that contributes to this pro-resolving reprogramming is the cargo that is released from apoptotic cells after their engulfment and phagolysosomal digestion by macrophages. The apoptotic cell cargo contains amino acids, nucleotides, fatty acids, and cholesterol that function as metabolites and signaling molecules to bring about this re-programming. Here, we review efferocytosis-induced changes in macrophage metabolism that mediate the pro-resolving functions of macrophages. We also discuss various strategies, challenges, and future perspectives related to drugging efferocytosis-fueled macrophage metabolism as strategy to dampen inflammation and promote resolution in chronic inflammatory diseases.
    MeSH term(s) Humans ; Apoptosis ; Phagocytosis ; Macrophages/metabolism ; Inflammation/metabolism ; Necrosis/metabolism
    Language English
    Publishing date 2023-05-09
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 391796-4
    ISSN 1600-065X ; 0105-2896
    ISSN (online) 1600-065X
    ISSN 0105-2896
    DOI 10.1111/imr.13214
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  9. Article ; Online: PFKFB2-mediated glycolysis promotes lactate-driven continual efferocytosis by macrophages.

    Schilperoort, Maaike / Ngai, David / Katerelos, Marina / Power, David A / Tabas, Ira

    Nature metabolism

    2023  Volume 5, Issue 3, Page(s) 431–444

    Abstract: Resolving-type macrophages prevent chronic inflammation by clearing apoptotic cells through efferocytosis. These macrophages are thought to rely mainly on oxidative phosphorylation, but emerging evidence suggests a possible link between efferocytosis and ...

    Abstract Resolving-type macrophages prevent chronic inflammation by clearing apoptotic cells through efferocytosis. These macrophages are thought to rely mainly on oxidative phosphorylation, but emerging evidence suggests a possible link between efferocytosis and glycolysis. To gain further insight into this issue, we investigated molecular-cellular mechanisms involved in efferocytosis-induced macrophage glycolysis and its consequences. We found that efferocytosis promotes a transient increase in macrophage glycolysis that is dependent on rapid activation of the enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 2 (PFKFB2), which distinguishes this process from glycolysis in pro-inflammatory macrophages. Mice transplanted with activation-defective PFKFB2 bone marrow and then subjected to dexamethasone-induced thymocyte apoptosis exhibit impaired thymic efferocytosis, increased thymic necrosis, and lower expression of the efferocytosis receptors MerTK and LRP1 on thymic macrophages compared with wild-type control mice. In vitro mechanistic studies revealed that glycolysis stimulated by the uptake of a first apoptotic cell promotes continual efferocytosis through lactate-mediated upregulation of MerTK and LRP1. Thus, efferocytosis-induced macrophage glycolysis represents a unique metabolic process that sustains continual efferocytosis in a lactate-dependent manner. The differentiation of this process from inflammatory macrophage glycolysis raises the possibility that it could be therapeutically enhanced to promote efferocytosis and resolution in chronic inflammatory diseases.
    MeSH term(s) Animals ; Mice ; c-Mer Tyrosine Kinase/metabolism ; Inflammation/metabolism ; Lactic Acid/metabolism ; Macrophages/metabolism ; Phagocytosis/physiology
    Chemical Substances c-Mer Tyrosine Kinase (EC 2.7.10.1) ; Lactic Acid (33X04XA5AT) ; Pfkfb2 protein, mouse (EC 2.7.1.105)
    Language English
    Publishing date 2023-02-16
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2522-5812
    ISSN (online) 2522-5812
    DOI 10.1038/s42255-023-00736-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  10. Article ; Online: Cardiology: Bad matters made worse.

    Tabas, Ira

    Nature

    2012  Volume 487, Issue 7407, Page(s) 306–308

    MeSH term(s) Animals ; Atherosclerosis/etiology ; Atherosclerosis/pathology ; Myocardial Infarction/complications ; Myocardial Infarction/pathology
    Language English
    Publishing date 2012-07-18
    Publishing country England
    Document type News ; Comment
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/487306a
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

To top