Evidence map›Paper›PMID 39968501›Full record

ArticleMedComm2025

Histidine triad nucleotide-binding protein 2 attenuates doxorubicin-induced cardiotoxicity through restoring lysosomal function and promoting autophagy in mice.

Hao Jiang, Jinyan Zhang, Daile Jia, Liwei Liu, Jinfeng Gao, Beijian Zhang, Zhen Dong, Xiaolei Sun, Wenlong Yang, Tiantong Ou and 6 more

Abstract read
In one paragraph

Article in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Review
  3. Mitochondrial tRNAHuman mutation · 2026
    Article
  4. Review
  5. Article
  6. 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

16 authors.

Hao JiangDepartment of Cardiology Zhongshan Hospital Fudan University Shanghai Institute of Cardiovascular Diseases Shanghai Shanghai China.
Jinyan ZhangDepartment of Cardiology Zhongshan Hospital Fudan University Shanghai Institute of Cardiovascular Diseases Shanghai Shanghai China.
Daile JiaDepartment of Cardiology Zhongshan Hospital Fudan University Shanghai Institute of Cardiovascular Diseases Shanghai Shanghai China.
Liwei LiuDepartment of Cardiology Zhongshan Hospital Fudan University Shanghai Institute of Cardiovascular Diseases Shanghai Shanghai China.
Jinfeng GaoDepartment of Cardiology Zhongshan Hospital Fudan University Shanghai Institute of Cardiovascular Diseases Shanghai Shanghai China.
Beijian ZhangDepartment of Cardiology Zhongshan Hospital Fudan University Shanghai Institute of Cardiovascular Diseases Shanghai Shanghai China.
Zhen DongDepartment of Cardiology Zhongshan Hospital Fudan University Shanghai Institute of Cardiovascular Diseases Shanghai Shanghai China.
Xiaolei SunDepartment of Cardiology Zhongshan Hospital Fudan University Shanghai Institute of Cardiovascular Diseases Shanghai Shanghai China.
Wenlong YangDepartment of Cardiology Zhongshan Hospital Fudan University Shanghai Institute of Cardiovascular Diseases Shanghai Shanghai China.
Tiantong OuDepartment of Cardiology Zhongshan Hospital Fudan University Shanghai Institute of Cardiovascular Diseases Shanghai Shanghai China.
Suling DingDepartment of Cardiology Zhongshan Hospital Fudan University Shanghai Institute of Cardiovascular Diseases Shanghai Shanghai China.
Luna HeDepartment of Nephrology Zhongshan Hospital Fudan University Shanghai China.
Yiqin ShiDepartment of Nephrology Zhongshan Hospital Fudan University Shanghai China.
Kai HuDepartment of Cardiology Zhongshan Hospital Fudan University Shanghai Institute of Cardiovascular Diseases Shanghai Shanghai China.
Aijun SunDepartment of Cardiology Zhongshan Hospital Fudan University Shanghai Institute of Cardiovascular Diseases Shanghai Shanghai China.
Junbo GeDepartment of Cardiology Zhongshan Hospital Fudan University Shanghai Institute of Cardiovascular Diseases Shanghai Shanghai China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Doxorubicin (DOX) is an effective chemotherapy drug widely used against various cancers but is limited by severe cardiotoxicity. Mitochondria-lysosome interactions are crucial for cellular homeostasis. This study investigates the role of histidine triad nucleotide-binding protein 2 (HINT2) in DOX-induced cardiotoxicity (DIC). We found that HINT2 expression was significantly upregulated in the hearts of DOX-treated mice. Cardiac-specific

Indexed as

autophagydoxorubicinHINT2lysosomeNAD+/NADH

Identifiers

PMID39968501
PMCPMC11831189

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.