Evidence map›Paper›PMID 35203316›Full record

ArticleCells2022

Administration of an Acidic Sphingomyelinase (ASMase) Inhibitor, Imipramine, Reduces Hypoglycemia-Induced Hippocampal Neuronal Death.

A Ra Kho, Bo Young Choi, Song Hee Lee, Dae Ki Hong, Beom Seok Kang, Si Hyun Lee, Sang Won Suh

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

A Ra KhoDepartment of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Kangwon-do, Korea.
Bo Young ChoiDepartment of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Kangwon-do, Korea.ORCID 0000-0002-9579-3503
Song Hee LeeDepartment of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Kangwon-do, Korea.
Dae Ki HongDepartment of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Kangwon-do, Korea.
Beom Seok KangDepartment of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Kangwon-do, Korea.
Si Hyun LeeDepartment of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Kangwon-do, Korea.
Sang Won SuhDepartment of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Kangwon-do, Korea.
Hallym University · KR

Funding

Hallym University Research Fund HRF-202012-015National Research Foundation of Korea National Research Foundation of KoreaNational Research Foundation of Korea NRF-2020R1A6A3A01096433
6 · The paper itself

Abstract

Severe hypoglycemia (below 35 mg/dL) appears most often in diabetes patients who continuously inject insulin. To rapidly cease the hypoglycemic state in this study, glucose reperfusion was conducted, which can induce a secondary neuronal death cascade following hypoglycemia. Acid sphingomyelinase (ASMase) hydrolyzes sphingomyelin into ceramide and phosphorylcholine. ASMase activity can be influenced by cations, pH, redox, lipids, and other proteins in the cells, and there are many changes in these factors in hypoglycemia. Thus, we expect that ASMase is activated excessively after hypoglycemia. Ceramide is known to cause free radical production, excessive inflammation, calcium dysregulation, and lysosomal injury, resulting in apoptosis and the necrosis of neurons. Imipramine is mainly used in the treatment of depression and certain anxiety disorders, and it is particularly known as an ASMase inhibitor. We hypothesized that imipramine could decrease hippocampal neuronal death by reducing ceramide via the inhibition of ASMase after hypoglycemia. In the present study, we confirmed that the administration of imipramine significantly reduced hypoglycemia-induced neuronal death and improved cognitive function. Therefore, we suggest that imipramine may be a promising therapeutic tool for preventing hypoglycemia-induced neuronal death.

Indexed as

HypoglycemiaImipramineCeramidesHippocampusHumansSphingomyelin PhosphodiesteraseCeramidesImipramineSphingomyelin Phosphodiesteraseacidic sphingomyelinaseceramidecognitive dysfunctionhypoglycemiaimipramineneuron deathsphingolipid

Identifiers

PMID35203316
PMCPMC8869983
OpenAlexW4213099893

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.