Evidence map›Paper›PMID 37860639›Full record

ArticleChemical science2023

Targeting mitochondrial degradation by chimeric autophagy-tethering compounds.

Zhenqi Liu, Geng Qin, Jie Yang, Wenjie Wang, Wenting Zhang, Boxun Lu, Jinsong Ren, Xiaogang Qu

Open access · diamondAbstract read
In one paragraph

Article in Chemical science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Review
  3. Autophagy modulation in cancer.Nature reviews. Drug discovery · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Frontiers in nutrition · 2025
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
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

8 authors at 2 institutions in 1 country.

Zhenqi LiuLaboratory of Chemical Biology, State Key Laboratory of Rare Earth Resource Utilization, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences Changchun Jilin 130022 P. R. China xqu@ciac.ac.cn.
Geng QinLaboratory of Chemical Biology, State Key Laboratory of Rare Earth Resource Utilization, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences Changchun Jilin 130022 P. R. China xqu@ciac.ac.cn.
Jie YangLaboratory of Chemical Biology, State Key Laboratory of Rare Earth Resource Utilization, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences Changchun Jilin 130022 P. R. China xqu@ciac.ac.cn.
Wenjie WangLaboratory of Chemical Biology, State Key Laboratory of Rare Earth Resource Utilization, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences Changchun Jilin 130022 P. R. China xqu@ciac.ac.cn.
Wenting ZhangLaboratory of Chemical Biology, State Key Laboratory of Rare Earth Resource Utilization, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences Changchun Jilin 130022 P. R. China xqu@ciac.ac.cn.
Boxun LuNeurology Department at Huashan Hospital, State Key Laboratory of Medical Neurobiology, Ministry of Education Frontiers Center for Brain Science, School of Life Sciences, Fudan University Shanghai China luboxun@fudan.edu.cn.ORCID https://orcid.org/0000-0002-1675-9340
Jinsong RenLaboratory of Chemical Biology, State Key Laboratory of Rare Earth Resource Utilization, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences Changchun Jilin 130022 P. R. China xqu@ciac.ac.cn.ORCID https://orcid.org/0000-0002-7506-627X
Xiaogang QuLaboratory of Chemical Biology, State Key Laboratory of Rare Earth Resource Utilization, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences Changchun Jilin 130022 P. R. China xqu@ciac.ac.cn.ORCID https://orcid.org/0000-0003-2868-3205
University of Science and Technology of China · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ability to regulate mitophagy in a living system with small molecules remains a great challenge. We hypothesize that adding fragments specific to the key autophagosome protein LC3 to mitochondria will mimic receptor-mediated mitophagy, thus engaging the autophagy-lysosome pathway to induce mitochondrial degradation. Herein, we develop a general biochemical approach to modulate mitophagy, dubbed mito-ATTECs, which employ chimera molecules composed of LC3-binding moieties linked to mitochondria-targeting ligands. Mito-ATTECs trigger mitophagy

Identifiers

PMID37860639
PMCPMC10583747
OpenAlexW4387029271

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.