Evidence map›Paper›PMID 30213857›Full record

ArticleThe Journal of biological chemistry2018

Apoptotic β-cells induce macrophage reprogramming under diabetic conditions.

Meliza G Ward, Ge Li, Mingming Hao

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 28 citations in OpenAlex.

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  15. Whole Exome Sequencing Study in a Family with Type 2 Diabetes Mellitus.International journal of general medicine · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Meliza G WardFrom the Department of Biochemistry, Weill Medical College of Cornell University, New York, New York 10065.
Ge LiFrom the Department of Biochemistry, Weill Medical College of Cornell University, New York, New York 10065.
Mingming HaoFrom the Department of Biochemistry, Weill Medical College of Cornell University, New York, New York 10065 mhao@med.cornell.edu.ORCID 0000-0003-4677-5111
Cornell University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes mellitus (T2DM) occurs when insulin-producing pancreatic β-cells fail to secrete sufficient insulin to compensate for insulin resistance. As T2DM progresses, apoptotic β-cells need to be removed by macrophages through efferocytosis that is anti-inflammatory by nature. Paradoxically, infiltrating macrophages are a main source of inflammatory cytokines that leads to T2DM. It is unclear how apoptotic β-cells impact macrophage function. We show under diabetic conditions, phagocytosis of apoptotic β-cells causes lysosomal permeabilization and generates reactive oxygen species that lead to inflammasome activation and cytokine secretion in macrophages. Efferocytosis-induced lipid accumulation transforms islet macrophages into foam cell-like outside the context of atherosclerosis. Our study suggests that whereas macrophages normally play a protective anti-inflammatory role, the increasing demand of clearing apoptotic cells may trigger them to undergo proinflammatory reprogramming as T2DM progresses. This shift in the balance between opposing macrophage inflammatory responses could contribute to chronic inflammation involved in metabolic diseases. Our study highlights the importance of preserving macrophage lysosomal function as a therapeutic intervention for diabetes progression.

Indexed as

ApoptosisAnimalsCytokinesDiabetes Mellitus, Type 2HumansInflammationInsulin-Secreting CellsLysosomesMacrophagesReactive Oxygen SpeciesCytokinesReactive Oxygen Speciesapoptosisbeta cell (B-cell)diabetesglucoseinflammationisletlysosomemacrophage

Identifiers

PMID30213857
PMCPMC6200952
OpenAlexW2891767442

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.