Evidence map›Paper›PMID 32645929›Full record

ArticleInternational journal of molecular sciences2020

Acute Hyperglycemia Aggravates Lung Injury via Activation of the SGK1-NKCC1 Pathway.

Chin-Pyng Wu, Kun-Lun Huang, Chung-Kan Peng, Chou-Chin Lan

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

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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

14 citing papers in PubMed, 23 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

4 authors at 3 institutions in 1 country.

Chin-Pyng WuDepartment of Critical Care Medicine, Landseed International Hospital, Tao-Yuan 32449, Taiwan.
Kun-Lun HuangDivision of Pulmonary Medicine, National Defense Medical Center, Tri-Service General Hospital, Taipei 11490, Taiwan.
Chung-Kan PengDivision of Pulmonary Medicine, National Defense Medical Center, Tri-Service General Hospital, Taipei 11490, Taiwan.ORCID 0000-0001-5696-2557
Chou-Chin LanDivision of Pulmonary Medicine, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei City 23142, Taiwan.
Tri-Service General Hospital · TWLandseed Hospital · TWTzu Chi University · TW

Funding

Landseed Hospital LSH-2017-01Taipei Tzu Chi Hospital TCRD-TPE-106-11 and TCRD-TPE-109-24(1/3)
6 · The paper itself

Abstract

Acute lung injury (ALI) is characterized by severe hypoxemia and has significantly high mortality rates. Acute hyperglycemia occurs in patients with conditions such as sepsis or trauma, among others, and it results in aggravated inflammation and induces damage in patients with ALI. Regulation of alveolar fluid is essential for the development and resolution of pulmonary edema in lung injury. Pulmonary sodium-potassium-chloride co-transporter 1 (NKCC1) regulates the net influx of ions and water into alveolar cells. The activation of with-no-lysine kinase 4 (WNK4), STE20/SPS1-related proline/alanine rich kinase (SPAK) and the NKCC1 pathway lead to an increase in the expression of NKCC1 and aggravation of ALI. Moreover, hyperglycemia is known to induce NKCC1 expression via the activation of the serum-glucocorticoid kinase 1 (SGK1)-NKCC1 pathway. We aim to evaluate the influence of acute hyperglycemia on the SGK1-NKCC1 pathway in ALI. ALI was induced using a high tidal volume for four hours in a rat model. Acute hyperglycemia was induced by injection with 0.5 mL of 40% glucose solution followed by continuous infusion at 2 mL/h. The animals were divided into sham, sham+ hyperglycemia, ALI, ALI + hyperglycemia, ALI + inhaled bumetanide (NKCC1 inhibitor) pretreatment, ALI + hyperglycemia + inhalational bumetanide pretreatment, and ALI + hyperglycemia + post-ALI inhalational bumetanide groups. Severe lung injury along with pulmonary edema, alveolar protein leakage, and lung inflammation was observed in ALI with hyperglycemia than in ALI without hyperglycemia. This was concurrent with the higher expression of pro-inflammatory cytokines, infiltration of neutrophils and alveolar macrophages (AM) 1, and NKCC1 expression. Inhalational NKCC1 inhibitor significantly inhibited the SGK1-NKCC1, and WNK4-SPAK-NKCC1 pathways. Additionally, it reduced pulmonary edema, inflammation, levels of pro-inflammatory cytokines, neutrophils and AM1 and increased AM2. Therefore, acute hyperglycemia aggravates lung injury via the further activation of the SGK1-NKCC1 pathway. The NKCC1 inhibitor can effectively attenuate lung injury aggravated by acute hyperglycemia.

Indexed as

Acute Lung InjuryAlveolar Epithelial CellsAnimalsBumetanideHyperglycemiaImmediate-Early ProteinsLungMacrophages, AlveolarMalePneumoniaProtein Serine-Threonine KinasesPulmonary EdemaRatsRats, Sprague-DawleySerum-Glucocorticoid Regulated KinasesSignal TransductionBumetanideImmediate-Early ProteinsProtein Serine-Threonine KinasesSerum-Glucocorticoid Regulated KinasesSlc12a2 protein, ratSolute Carrier Family 12, Member 2acute lung injuryhyperglycemiaserum-glucocorticoid kinase 1sodium-potassium-chloride co-transporter isoform 1

Identifiers

PMID32645929
PMCPMC7370284
OpenAlexW3039527594

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.