Islet Macrophages Shift to a Reparative State following Pancreatic Beta-Cell Death and Are a Major Source of Islet Insulin-like Growth Factor-1 (Q92804882)

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scientific article published on 14 December 2019

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English	Islet Macrophages Shift to a Reparative State following Pancreatic Beta-Cell Death and Are a Major Source of Islet Insulin-like Growth Factor-1	scientific article published on 14 December 2019

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1 May 2020

Islet Macrophages Shift to a Reparative State following Pancreatic Beta-Cell Death and Are a Major Source of Islet Insulin-like Growth Factor-1 (English)

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1 May 2020

author name string

Dominika Nackiewicz

1

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1 May 2020

Meixia Dan

2

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1 May 2020

Madeleine Speck

3

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1 May 2020

Samuel Z Chow

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1 May 2020

Yi-Chun Chen

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J Andrew Pospisilik

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1 May 2020

C Bruce Verchere

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1 May 2020

Jan A Ehses

8

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14 December 2019

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23

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1 May 2020

1

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1 May 2020

100775

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1 May 2020

How macrophages deal with death

1 reference

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IGF-1 and cardiovascular disease

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Efferocytosis Fuels Requirements of Fatty Acid Oxidation and the Electron Transport Chain to Polarize Macrophages for Tissue Repair

1 reference

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Expansion of Islet-Resident Macrophages Leads to Inflammation Affecting β Cell Proliferation and Function in Obesity

1 reference

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Deciphering the Dynamic Transcriptional and Post-transcriptional Networks of Macrophages in the Healthy Heart and after Myocardial Injury

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Evidence against a role for NLRP3-driven islet inflammation in db/db mice.

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Tissue-Resident Macrophages Are Locally Programmed for Silent Clearance of Apoptotic Cells

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Effects of growth hormone on glucose metabolism and insulin resistance in human.

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The islet-resident macrophage is in an inflammatory state and senses microbial products in blood.

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Cell Removal: Efferocytosis

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Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells.

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Eating the Dead to Keep Atherosclerosis at Bay.

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Mechanisms of Organ Injury and Repair by Macrophages

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11 February 2021

Macrophages redirect phagocytosis by non-professional phagocytes and influence inflammation

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Insulitis in human diabetes: a histological evaluation of donor pancreases

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Chemoresistance in Pancreatic Cancer Is Driven by Stroma-Derived Insulin-Like Growth Factors

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Two years in IGF research

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Transient effects of empty liposomes on hepatic macrophage populations in rats

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Life and death of β cells in Type 1 diabetes: A comprehensive review

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Islet inflammation in type 2 diabetes

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Differential Activation of Innate Immune Pathways by Distinct Islet Amyloid Polypeptide (IAPP) Aggregates

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11 February 2021

Tissue biology perspective on macrophages

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The pancreas anatomy conditions the origin and properties of resident macrophages

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Macrophages are essential for CTGF-mediated adult β-cell proliferation after injury

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Monocyte/Macrophage-derived IGF-1 Orchestrates Murine Skeletal Muscle Regeneration and Modulates Autocrine Polarization

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TLR2/6 and TLR4-activated macrophages contribute to islet inflammation and impair beta cell insulin gene expression via IL-1 and IL-6

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Glycoprotein 130 receptor signaling mediates α-cell dysfunction in a rodent model of type 2 diabetes.

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TGFBI (βIG-H3) is a diabetes-risk gene based on mouse and human genetic studies

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Islet microenvironment, modulated by vascular endothelial growth factor-A signaling, promotes β cell regeneration

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Resident macrophages mediate islet amyloid polypeptide-induced islet IL-1β production and β-cell dysfunction.

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SHIP-deficient, alternatively activated macrophages protect mice during DSS-induced colitis.

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TGF-βi Promotes Islet β-Cell Function and Regeneration

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1 reference

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1 reference

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Immunosuppressive effects of apoptotic cells

1 reference

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1 reference

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1 reference

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11 February 2021

Identifiers

10.1016/J.ISCI.2019.100775

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1 May 2020

PMC publication ID

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1 May 2020

PubMed publication ID

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1 May 2020

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