Evidence map›Paper›PMID 41120260›Full record

ReviewCell death discovery2025

Mitochondrial orchestration of PANoptosis: mechanisms, disease pathogenesis, and emerging therapeutic frontiers.

Jiale Zhang, Xiaoya Fu, Feifan Jia, Yahao Jing, Jiameng Zhang, Aoxue Bai, Mengyuan Cui, Lei Zhang, Kunhou Yao

Abstract readReview
In one paragraph

Review in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
  2. A mitochondria-targeted HRedox biology · 2026
    Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Mitochondria-associated programmed cell death in pancreatic β cell of T2DM.Apoptosis : an international journal on programmed cell death · 2026
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. 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

9 authors.

Jiale Zhang *Department of General Surgery, the Second Clinical Medical College of Henan University (Huaihe Hospital), Henan University, Kaifeng, Henan, China.
Xiaoya Fu *School of Basic Medical Sciences, Henan University, Kaifeng, Henan, China.
Feifan JiaSchool of Basic Medical Sciences, Henan University, Kaifeng, Henan, China.
Yahao JingSchool of Basic Medical Sciences, Henan University, Kaifeng, Henan, China.
Jiameng ZhangSchool of Basic Medical Sciences, Henan University, Kaifeng, Henan, China.
Aoxue BaiSchool of Basic Medical Sciences, Henan University, Kaifeng, Henan, China.
Mengyuan CuiSchool of Basic Medical Sciences, Henan University, Kaifeng, Henan, China.
Lei ZhangDepartment of General Surgery, the Second Clinical Medical College of Henan University (Huaihe Hospital), Henan University, Kaifeng, Henan, China. zhlei@henu.edu.cn.ORCID http://orcid.org/0000-0002-7781-3478
Kunhou YaoDepartment of General Surgery, the Second Clinical Medical College of Henan University (Huaihe Hospital), Henan University, Kaifeng, Henan, China. yaokunhou@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria, traditionally known as cellular powerhouses, are now recognized as central regulators of programmed cell death (PCD) and key players in disease pathogenesis. This review synthesizes current knowledge on mitochondrial mechanisms in PANoptosis-a convergent pathway integrating apoptosis, necroptosis, and pyroptosis-and their implications in diverse pathologies. Mitochondria govern intrinsic apoptosis via Bcl-2 family proteins and mitochondrial outer membrane permeabilization (MOMP), amplify necroptosis through RIPK1/RIPK3-driven ROS signaling, and indirectly regulate pyroptosis via inflammasome-mitochondria crosstalk. Dysfunctional mitochondria contribute to neurodegenerative diseases, cardiovascular disorders, cancer, and autoimmune/metabolic syndromes. Emerging therapies targeting mitochondrial pathways, such as Bcl-2 inhibitors, mPTP modulators, and ROS-inducing agents, demonstrate clinical promise in restoring cell death sensitivity and mitigating inflammation. By bridging molecular mechanisms with therapeutic innovations, this work underscores mitochondria as dynamic hubs of cellular fate and disease intervention.

Identifiers

PMID41120260
PMCPMC12540656

What OpenQuestion 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 OpenQuestion graph.