Evidence map›Paper›PMID 35224007›Full record

ArticleKidney diseases (Basel, Switzerland)2022

Targeting Ferroptosis Attenuates Interstitial Inflammation and Kidney Fibrosis.

Lu Zhou, Xian Xue, Qing Hou, Chunsun Dai

Abstract read
In one paragraph

Article in Kidney diseases (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
–field-weighted citation impact
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

62 citing papers in PubMed.

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2 more citing papers are in PubMed but not listed here.

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.

Lu ZhouCenter for Kidney Disease, The Second Affiliated Hospital, Nanjing Medical University, Nanjing, China.
Xian XueDepartment of Clinical Genetics, The Second Affiliated Hospital, Nanjing Medical University, Nanjing, China.
Qing HouCenter for Kidney Disease, The Second Affiliated Hospital, Nanjing Medical University, Nanjing, China.
Chunsun DaiCenter for Kidney Disease, The Second Affiliated Hospital, Nanjing Medical University, Nanjing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFerroptosis, an iron-dependent form of regulated necrosis mediated by lipid peroxidation, predominantly polyunsaturated fatty acids, is involved in postischemic and toxic kidney injury. However, the role and mechanisms for tubular epithelial cell (TEC) ferroptosis in kidney fibrosis remain largely unknown.

objectivesThe aim of the study was to decipher the role and mechanisms for TEC ferroptosis in kidney fibrosis.

methodsMouse models with unilateral ureter obstruction (UUO) or ischemia/reperfusion injury (IRI) were generated.

resultsWe found that TEC ferroptosis exhibited as reduced glutathione peroxidase 4 (GPX4) expression and increased 4-hydroxynonenal abundance was appeared in kidneys from chronic kidney disease (CKD) patients and mouse models with UUO or IRI. Inhibition of ferroptosis could largely mitigate kidney injury, interstitial fibrosis, and inflammatory cell accumulation in mice after UUO or IRI. Additionally, treatment of TECs with (1S,3R)-RSL-3, an inhibitor of GPX4, could enhance cell ferroptosis and recruit macrophages. Furthermore, inhibiting TEC ferroptosis reduced monocyte chemotactic protein 1 (MCP-1) secretion and macrophage chemotaxis.

conclusionsThis study uncovers that TEC ferroptosis may promote interstitial fibrosis and inflammation, and targeting ferroptosis may shine a light on protecting against kidney fibrosis in patients with CKDs.

Indexed as

FerroptosisKidney fibrosisTubular cells

Identifiers

PMID35224007
PMCPMC8820137

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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.