Evidence map›Paper›PMID 25539831›Full record

ArticlePhysiological reports2014

Downregulation of cystathionine β-synthase and cystathionine γ-lyase expression stimulates inflammation in kidney ischemia-reperfusion injury.

Pengqi Wang, Cara K Isaak, Yaw L Siow, Karmin O

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Cysteine as a Multifaceted Player in Kidney, theMolecules (Basel, Switzerland) · 2022
    Review
  8. Article
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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.

Pengqi WangSt. Boniface Hospital Research Centre, Winnipeg, Manitoba, Canada Department of Animal Science, University of Manitoba, Winnipeg, Manitoba, Canada.
Cara K IsaakDepartment of Physiology, University of Manitoba, Winnipeg, Manitoba, Canada Agriculture and Agri Food Canada, Winnipeg, Manitoba, Canada.
Yaw L SiowSt. Boniface Hospital Research Centre, Winnipeg, Manitoba, Canada Department of Physiology, University of Manitoba, Winnipeg, Manitoba, Canada Agriculture and Agri Food Canada, Winnipeg, Manitoba, Canada.
Karmin OSt. Boniface Hospital Research Centre, Winnipeg, Manitoba, Canada Department of Animal Science, University of Manitoba, Winnipeg, Manitoba, Canada Department of Physiology, University of Manitoba, Winnipeg, Manitoba, Canada.
St. Boniface Hospital · CAAgriculture and Agri-Food Canada · CAUniversity of Manitoba · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation plays a critical role in kidney ischemia-reperfusion injury but mechanisms of increased proinflammatory cytokine expression are not completely understood. Kidney has a high expression of cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CSE) that can synthesize hydrogen sulfide. CBE and CSE are also responsible for the synthesis of cysteine, an essential precursor for glutathione, an antioxidant. Reduced hydrogen sulfide and glutathione production is associated with multiple organ injury. Although pro- and anti-inflammatory effects of hydrogen sulfide have been reported, its role in ischemia-reperfusion-induced inflammation in the kidney has not been well addressed. The aim of this study was to investigate the effect of CBS and CSE-mediated hydrogen sulfide and glutathione production on kidney inflammatory response and the mechanism involved. The left kidney of Sprague-Dawley rat was subjected to 45-min ischemia followed by reperfusion for 24 h. Ischemia-reperfusion caused a significant decrease in CBS and CSE mRNA and protein levels with a concomitant reduction of glutathione and hydrogen sulfide production in the kidney while the expression of proinflammatory cytokine expression (MCP-1, IL-6) was elevated. Hypoxia-reoxygenation of proximal tubular cells led to a decrease in CBS and CSE expression and an increase in proinflammatory cytokine expression. Supplementation of glutathione or hydrogen sulfide donor (NaHS) effectively attenuated cytokine expression in tubular cells. These results suggested that ischemia-reperfusion impaired CBS and CSE-mediated glutathione and hydrogen sulfide production in the kidney, which augmented the expression of proinflammatory cytokines. Regulation of CBS and CSE expression may be therapeutically relevant in alleviating ischemia-reperfusion-induced inflammation and improving kidney function.

Indexed as

Cystathionine‐beta‐synthasecystathionine‐gamma‐lyasehydrogen sulfideinflammationischemia–reperfusionkidney

Identifiers

PMID25539831
PMCPMC4332225
OpenAlexW2162788150

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.