Evidence map›Paper›PMID 39281670›Full record

ReviewFrontiers in immunology2024

Unravelling oncosis: morphological and molecular insights into a unique cell death pathway.

Jie Guo, Wen-Tao Yang, Feng-Yi Mai, Jing-Rong Liang, Jiao Luo, Ming-Chao Zhou, Dong-Dong Yu, Yu-Long Wang, Chen-Guang Li

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
–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

11 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Metabolic starvation-induced cell swelling drives solid stress in tumors.bioRxiv : the preprint server for biology · 2026
    Article
  8. Review
  9. Review
  10. Article
  11. AssessingFrontiers in immunology · 2025
    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.

Jie Guo *Department of Rehabilitation Medicine, Shenzhen Second People's Hospital, Shenzhen, China.
Wen-Tao Yang *Pain Department of Huazhong University of Science and Technology Union Shenzhen Hospital (Nanshan Hospital), Shenzhen, China.
Feng-Yi Mai *Department of Human Cell Biology and Genetics, Southern University of Science and Technology School of Medicine, Shenzhen, China.
Jing-Rong LiangPain Department of Huazhong University of Science and Technology Union Shenzhen Hospital (Nanshan Hospital), Shenzhen, China.
Jiao LuoDepartment of Rehabilitation Medicine, Shenzhen Second People's Hospital, Shenzhen, China.
Ming-Chao ZhouDepartment of Rehabilitation Medicine, Shenzhen Second People's Hospital, Shenzhen, China.
Dong-Dong YuDepartment of Rehabilitation Medicine, Shenzhen Second People's Hospital, Shenzhen, China.
Yu-Long WangDepartment of Rehabilitation Medicine, Shenzhen Second People's Hospital, Shenzhen, China.
Chen-Guang LiPain Department of Huazhong University of Science and Technology Union Shenzhen Hospital (Nanshan Hospital), Shenzhen, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Programmed cell death (PCD) is a fundamental biological process for maintaining cellular equilibrium and regulating development, health, and disease across all living organisms. Among the various types of PCD, apoptosis plays a pivotal role in numerous diseases, notably cancer. Cancer cells frequently develop mechanisms to evade apoptosis, increasing resistance to standard chemotherapy treatments. This resistance has prompted extensive research into alternative mechanisms of programmed cell death. One such pathway is oncosis, characterized by significant energy consumption, cell swelling, dilation of the endoplasmic reticulum, mitochondrial swelling, and nuclear chromatin aggregation. Recent research suggests that oncosis can impact conditions such as chemotherapeutic cardiotoxicity, myocardial ischemic injury, stroke, and cancer, mediated by specific oncosis-related proteins. In this review, we provide a detailed examination of the morphological and molecular features of oncosis and discuss various natural or small molecule compounds that can induce this type of cell death. Additionally, we summarize the current understanding of the molecular mechanisms underlying oncosis and its role in both normal physiology and pathological conditions. These insights aim to illuminate future research directions and propose innovative strategies for leveraging oncosis as a therapeutic tool against human diseases and cancer resistance.

Indexed as

ApoptosisNeoplasmsAnimalsCell DeathHumansMitochondriaSignal Transductioncell deathdiseases and therapiesinducermechanismsoncosis

Identifiers

PMID39281670
PMCPMC11393741

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.