Evidence map›Paper›PMID 37568009›Full record

ArticleCell death and differentiation2023

FBXL4 mutations cause excessive mitophagy via BNIP3/BNIP3L accumulation leading to mitochondrial DNA depletion syndrome.

Yingji Chen, Dongyue Jiao, Yang Liu, Xiayun Xu, Yilin Wang, Xiaona Luo, Hexige Saiyin, Yao Li, Kun Gao, Yucai Chen and 3 more

Open access · greenAbstract read
In one paragraph

Article in Cell death and differentiation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Selective autophagy in kidney health and disease.Nature reviews. Nephrology · 2026
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  6. Sustained loss ofbioRxiv : the preprint server for biology · 2026
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  7. Identification and Screening of Lactate-Related Genes as Molecular Markers for Early Diagnosis of Steroid-Induced Osteonecrosis of the Femoral Head.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Targeting mitophagy in neurodegenerative diseases.Nature reviews. Drug discovery · 2025
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

13 authors at 4 institutions in 1 country.

Yingji Chen *Obstetrics & Gynecology Hospital of Fudan University, Institutes of Metabolism and Integrative Biology, State Key Laboratory of Genetic Engineering, MOE Engineering Research Center of Gene Technology, School of Life Sciences, Fudan University, Shanghai, PR China.
Dongyue Jiao *Obstetrics & Gynecology Hospital of Fudan University, Institutes of Metabolism and Integrative Biology, State Key Laboratory of Genetic Engineering, MOE Engineering Research Center of Gene Technology, School of Life Sciences, Fudan University, Shanghai, PR China.
Yang Liu *Department of Anatomy, Histology & Embryology, School of Basic Medical Science, Fudan University, Shanghai, PR China.
Xiayun XuObstetrics & Gynecology Hospital of Fudan University, Institutes of Metabolism and Integrative Biology, State Key Laboratory of Genetic Engineering, MOE Engineering Research Center of Gene Technology, School of Life Sciences, Fudan University, Shanghai, PR China.
Yilin WangDepartment of Neurology, Shanghai Children's Hospital, School of Medicine, Shanghai JiaoTong University, Shanghai, PR China.
Xiaona LuoDepartment of Neurology, Shanghai Children's Hospital, School of Medicine, Shanghai JiaoTong University, Shanghai, PR China.
Hexige SaiyinState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, PR China.ORCID 0000-0003-2993-6817
Yao LiObstetrics & Gynecology Hospital of Fudan University, Institutes of Metabolism and Integrative Biology, State Key Laboratory of Genetic Engineering, MOE Engineering Research Center of Gene Technology, School of Life Sciences, Fudan University, Shanghai, PR China.ORCID 0000-0001-5257-7272
Kun GaoDepartment of Clinical Laboratory, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, PR China.ORCID 0000-0001-9060-3881
Yucai ChenDepartment of Neurology, Shanghai Children's Hospital, School of Medicine, Shanghai JiaoTong University, Shanghai, PR China. chenyc@shchildren.com.cn.
Shi-Min ZhaoObstetrics & Gynecology Hospital of Fudan University, Institutes of Metabolism and Integrative Biology, State Key Laboratory of Genetic Engineering, MOE Engineering Research Center of Gene Technology, School of Life Sciences, Fudan University, Shanghai, PR China. zhaosm@fudan.edu.cn.ORCID 0000-0002-3674-9107
Lixiang MaDepartment of Anatomy, Histology & Embryology, School of Basic Medical Science, Fudan University, Shanghai, PR China. lxma@fudan.edu.cn.
Chenji WangObstetrics & Gynecology Hospital of Fudan University, Institutes of Metabolism and Integrative Biology, State Key Laboratory of Genetic Engineering, MOE Engineering Research Center of Gene Technology, School of Life Sciences, Fudan University, Shanghai, PR China. chenjiwang@fudan.edu.cn.ORCID 0000-0002-5752-6439
Fudan University · CNShanghai Jiao Tong University · CNShanghai First Maternity and Infant Hospital · CNShanghai Medical College of Fudan University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31821002, 31930062National Natural Science Foundation of China (National Science Foundation of China) 82071269National Natural Science Foundation of China (National Science Foundation of China) 82272992 and 91954106National Natural Science Foundation of China (National Science Foundation of China) No. 91957125, 81972396
6 · The paper itself

Abstract

Mitochondria are essential organelles found in eukaryotic cells that play a crucial role in ATP production through oxidative phosphorylation (OXPHOS). Mitochondrial DNA depletion syndrome (MTDPS) is a group of genetic disorders characterized by the reduction of mtDNA copy number, leading to deficiencies in OXPHOS and mitochondrial functions. Mutations in FBXL4, a substrate-binding adaptor of Cullin 1-RING ubiquitin ligase complex (CRL1), are associated with MTDPS, type 13 (MTDPS13). Here, we demonstrate that, FBXL4 directly interacts with the mitophagy cargo receptors BNIP3 and BNIP3L, promoting their degradation through the ubiquitin-proteasome pathway via the assembly of an active CRL1

Indexed as

F-Box ProteinsMembrane ProteinsMitophagyMutationProto-Oncogene ProteinsAnimalsDNA, MitochondrialHEK293 CellsHumansInduced Pluripotent Stem CellsMiceMitochondriaMitochondrial ProteinsTumor Suppressor ProteinsUbiquitin-Protein LigasesBNIP3L protein, humanBNIP3 protein, humanDNA, MitochondrialF-Box ProteinsFbxL4 protein, humanMembrane ProteinsMitochondrial ProteinsProto-Oncogene ProteinsTumor Suppressor ProteinsUbiquitin-Protein Ligases

Identifiers

PMID37568009
PMCPMC10589232
OpenAlexW4385753858

What OpenQuestion holds

Textmetadata
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.