Evidence map›Paper›PMID 39300060›Full record

ArticleNature communications2024

MFSD7C protects hemolysis-induced lung impairments by inhibiting ferroptosis.

Huirui Wang, Xiaona You, Jingcheng Wang, Xinyi Chen, Yinghui Gao, Mengmeng Wang, Wenru Zhang, Jiaozhen Zhang, Yang Yu, Bo Han and 4 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. More than a ring: the emerging role of heme in angiogenesis.Cell communication and signaling : CCS · 2026
    Review
  3. Article
  4. Article
  5. Article
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

14 authors.

Huirui Wang *Department of Natural Products Chemistry, Key Lab of Chemical Biology of the Ministry of Education, Shandong University, Jinan, China.ORCID 0009-0005-1907-6448
Xiaona You *Institute of Immunopharmaceutical Sciences, School of Pharmaceutical Sciences, Shandong University, Jinan, China.ORCID 0000-0001-9996-1466
Jingcheng Wang *Department of Natural Products Chemistry, Key Lab of Chemical Biology of the Ministry of Education, Shandong University, Jinan, China.
Xinyi ChenDivision of Infection and Immunity, University College London, London, USA.
Yinghui GaoDepartment of Natural Products Chemistry, Key Lab of Chemical Biology of the Ministry of Education, Shandong University, Jinan, China.
Mengmeng WangDepartment of Natural Products Chemistry, Key Lab of Chemical Biology of the Ministry of Education, Shandong University, Jinan, China.
Wenru ZhangDepartment of Natural Products Chemistry, Key Lab of Chemical Biology of the Ministry of Education, Shandong University, Jinan, China.
Jiaozhen ZhangDepartment of Natural Products Chemistry, Key Lab of Chemical Biology of the Ministry of Education, Shandong University, Jinan, China.
Yang YuAdvanced Medical Research Institute, Cheeloo College of Medicine, Shandong University, Jinan, China.
Bo HanDepartment of Pathology, Shandong University School of Basic Medical Sciences, Jinan, China.
Mei QiDepartment of Pathology, Shandong University Qilu hospital, Jinan, China.
Xiaohui LiuState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. xiaohuiliu@imm.ac.cn.ORCID 0009-0003-1058-5444
Hongxiang LouDepartment of Natural Products Chemistry, Key Lab of Chemical Biology of the Ministry of Education, Shandong University, Jinan, China. louhongxiang@sdu.edu.cn.ORCID 0000-0003-3300-1811
Ting DongDepartment of Natural Products Chemistry, Key Lab of Chemical Biology of the Ministry of Education, Shandong University, Jinan, China. dongting2016@gmail.com.ORCID 0000-0003-2159-7937

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82100185National Natural Science Foundation of China (National Science Foundation of China) 82204404
6 · The paper itself

Abstract

Hemolysis drives susceptibility to lung injury and predicts poor outcomes in diseases, such as malaria and sickle cell disease (SCD). However, the underlying pathological mechanism remains elusive. Here, we report that major facilitator superfamily domain containing 7 C (MFSD7C) protects the lung from hemolytic-induced damage by preventing ferroptosis. Mechanistically, MFSD7C deficiency in HuLEC-5A cells leads to mitochondrial dysfunction, lipid remodeling and dysregulation of ACSL4 and GPX4, thereby enhancing lipid peroxidation and promoting ferroptosis. Furthermore, systemic administration of MFSD7C mRNA-loaded nanoparticles effectively prevents lung injury in hemolytic mice, such as HbSS-Townes mice and PHZ-challenged 7 C

Indexed as

FerroptosisHemolysisMice, KnockoutPhospholipid Hydroperoxide Glutathione PeroxidaseAnemia, Sickle CellAnimalsCoenzyme A LigasesDisease Models, AnimalFemaleHumansLipid PeroxidationLungLung InjuryMaleMembrane Transport ProteinsMiceAcsl4 protein, mouseCoenzyme A LigasesFLVCR2 protein, humanglutathione peroxidase 4, mouseMembrane Transport ProteinsPhospholipid Hydroperoxide Glutathione PeroxidaseReceptors, Virus

Identifiers

PMID39300060
PMCPMC11413235

What OpenQuestion holds

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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.