Evidence map›Paper›PMID 36361505›Full record

ReviewInternational journal of molecular sciences2022

Necroptosis: A Pathogenic Negotiator in Human Diseases.

Hitesh Singh Chaouhan, Ch Vinod, Nikita Mahapatra, Shao-Hua Yu, I-Kuan Wang, Kuen-Bao Chen, Tung-Min Yu, Chi-Yuan Li

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
5.3field-weighted citation impact, top 3% 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

41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 64 citations in OpenAlex.

  1. Metabolic cell death in cancer: mechanisms and therapeutic potential.Apoptosis : an international journal on programmed cell death · 2025
    Pooled it
  2. Pooled it
  3. Necroptosis in Down Syndrome.Cell death & disease · 2026
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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 2 countries.

Hitesh Singh ChaouhanGraduate Institute of Biomedical Sciences, China Medical University, Taichung 40402, Taiwan.
Ch VinodDepartment of Biological Sciences, School of Applied Sciences, KIIT University, Bhubaneshwar 751024, India.
Nikita MahapatraDepartment of Biological Sciences, School of Applied Sciences, KIIT University, Bhubaneshwar 751024, India.
Shao-Hua YuDepartment of Emergency Medicine, China Medical University Hospital, Taichung 40402, Taiwan.ORCID 0000-0003-1072-7935
I-Kuan WangSchool of Medicine, China Medical University, Taichung 40402, Taiwan.
Kuen-Bao ChenDepartment of Anesthesiology, China Medical University Hospital, Taichung 40402, Taiwan.
Tung-Min YuSchool of Medicine, China Medical University, Taichung 40402, Taiwan.
Chi-Yuan LiGraduate Institute of Biomedical Sciences, China Medical University, Taichung 40402, Taiwan.
China Medical University · TWKIIT University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over the past few decades, mechanisms of programmed cell death have attracted the scientific community because they are involved in diverse human diseases. Initially, apoptosis was considered as a crucial mechanistic pathway for programmed cell death; recently, an alternative regulated mode of cell death was identified, mimicking the features of both apoptosis and necrosis. Several lines of evidence have revealed that dysregulation of necroptosis leads to pathological diseases such as cancer, cardiovascular, lung, renal, hepatic, neurodegenerative, and inflammatory diseases. Regulated forms of necrosis are executed by death receptor ligands through the activation of receptor-interacting protein kinase (RIPK)-1/3 and mixed-lineage kinase domain-like (MLKL), resulting in the formation of a necrosome complex. Many papers based on genetic and pharmacological studies have shown that RIPKs and MLKL are the key regulatory effectors during the progression of multiple pathological diseases. This review focused on illuminating the mechanisms underlying necroptosis, the functions of necroptosis-associated proteins, and their influences on disease progression. We also discuss numerous natural and chemical compounds and novel targeted therapies that elicit beneficial roles of necroptotic cell death in malignant cells to bypass apoptosis and drug resistance and to provide suggestions for further research in this field.

Indexed as

NecroptosisReceptor-Interacting Protein Serine-Threonine KinasesApoptosisCell DeathHumansNecrosisProtein KinasesProtein KinasesReceptor-Interacting Protein Serine-Threonine Kinasesapoptosishuman diseasesMLKLnecroptosisRIPK1RIPK3

Identifiers

PMID36361505
PMCPMC9655262
OpenAlexW4307265269

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.