Evidence map›Paper›PMID 40277323›Full record

ArticleAutophagy2025

SMAD3 and PINK1 constitute a new positive feedback loop in regulation of mitophagy.

Mingzhu Tang, Guang Lu, Han-Ming Shen

Abstract read
In one paragraph

Article in Autophagy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Biomolecules · 2025
    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

3 authors.

Mingzhu TangFaculty of Healthy Sciences, Ministry of Education Frontiers Science Center for Precision Oncology, University of Macau, Macau, China.
Guang LuDepartment of Physiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.ORCID 0000-0002-2268-1033
Han-Ming ShenFaculty of Healthy Sciences, Ministry of Education Frontiers Science Center for Precision Oncology, University of Macau, Macau, China.ORCID 0000-0001-7369-5227

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitophagy, selective degradation of dysfunctional mitochondria by the autophagy-lysosome pathway, is critical for maintaining cellular homeostasis. In recent years, significant progress has been made in understanding how PINK1 (PTEN-induced kinase 1)-mediated phosphorylation and the E3 ubiquitin (Ub) ligase (PRKN/parkin)-mediated ubiquitination form a positive feedforward loop in control of mitophagy. Nevertheless, a fundamental question remains: How is PINK1 transcriptionally modulated under mitochondrial stress to finely support mitophagy? Recently, we unveiled a novel mechanism in control of

Indexed as

Feedback, PhysiologicalMitophagyProtein KinasesSmad3 ProteinAnimalsHumansMitochondriaModels, BiologicalPhosphorylationPTEN-Induced Putative KinaseSignal TransductionTransforming Growth Factor betaUbiquitin-Protein LigasesProtein KinasesPTEN-Induced Putative KinaseSmad3 ProteinTransforming Growth Factor betaUbiquitin-Protein LigasesMitophagyphosphorylationPINK1SMAD3transcription

Identifiers

PMID40277323
PMCPMC12363504

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.