Evidence map›Paper›PMID 30665344›Full record

ReviewJournal of translational medicine2019

Mechanisms by which hydrogen sulfide attenuates muscle function following ischemia-reperfusion injury: effects on Akt signaling, mitochondrial function, and apoptosis.

Michael D Wetzel, Joseph C Wenke

Open access · goldAbstract readReview
In one paragraph

Review in Journal of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.2field-weighted citation impact, top 15% 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

8 citing papers in PubMed, 29 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

2 authors at 1 institution in 1 country.

Michael D WetzelUS Army Institute of Surgical Research, Extremity Trauma and Regenerative Medicine, 3698 Chambers Pass BLDG 3611, Ft. Sam Houston, San Antonio, TX, 78234, USA.ORCID 0000-0001-8428-9152
Joseph C WenkeUS Army Institute of Surgical Research, Extremity Trauma and Regenerative Medicine, 3698 Chambers Pass BLDG 3611, Ft. Sam Houston, San Antonio, TX, 78234, USA. joseph.c.wenke.civ@mail.mil.
United States Army Institute of Surgical Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemia-reperfusion injury is caused by a period of ischemia followed by massive blood flow into a tissue that had experienced restricted blood flow. The severity of the injury is dependent on the time the tissue was restricted from blood flow, becoming more severe after longer ischemia times. This can lead to many complications such as tissue necrosis, cellular apoptosis, inflammation, metabolic and mitochondrial dysfunction, and even organ failure. One of the emerging therapies to combat ischemic reperfusion injury complications is hydrogen sulfide, which is a gasotransmitter that diffuses across cell membranes to exert effects on various signaling pathways regulating cell survival such as Akt, mitochondrial activity, and apoptosis. Although commonly thought of as a toxic gas, low concentrations of hydrogen sulfide have been shown to be beneficial in promoting tissue survival post-ischemia, and modulate a wide variety of cellular responses. This review will detail the mechanisms of hydrogen sulfide in affecting the Akt signaling pathway, mitochondrial function, and apoptosis, particularly in regards to ischemic reperfusion injury in muscle tissue. It will conclude with potential clinical applications of hydrogen sulfide, combinations with other therapies, and perspectives for future studies.

Indexed as

AnimalsApoptosisHumansHydrogen SulfideMitochondriaMusclesProto-Oncogene Proteins c-aktReperfusion InjurySignal TransductionHydrogen SulfideProto-Oncogene Proteins c-aktAktApoptosiseNOSHydrogen sulfideIschemia reperfusion injuryMitochondriaMuscle

Identifiers

PMID30665344
PMCPMC6340183
OpenAlexW2935864440

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.