Evidence map›Paper›PMID 41518404›Full record

ReviewApoptosis : an international journal on programmed cell death2026

Programmed cell death of keratinocytes: an active driver in psoriasis.

Tianyi Yuwen, Jingyu Tian, Yujie Chen, Zizhen Zhou, Ni Lian, Xu Chen

Abstract readReview
PubMed Publisher
In one paragraph

Review in Apoptosis : an international journal on programmed cell death, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

6 authors.

Tianyi YuwenJiangsu Provincial Key Laboratory of Dermatology, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, 12 Jiangwangmiao St., Nanjing, 210042, People's Republic of China.
Jingyu TianJiangsu Provincial Key Laboratory of Dermatology, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, 12 Jiangwangmiao St., Nanjing, 210042, People's Republic of China.
Yujie ChenJiangsu Provincial Key Laboratory of Dermatology, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, 12 Jiangwangmiao St., Nanjing, 210042, People's Republic of China.
Zizhen ZhouJiangsu Provincial Key Laboratory of Dermatology, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, 12 Jiangwangmiao St., Nanjing, 210042, People's Republic of China.
Ni LianJiangsu Provincial Key Laboratory of Dermatology, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, 12 Jiangwangmiao St., Nanjing, 210042, People's Republic of China. lianni@aliyun.com.
Xu ChenJiangsu Provincial Key Laboratory of Dermatology, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, 12 Jiangwangmiao St., Nanjing, 210042, People's Republic of China. chenx@pumcderm.cams.cn.ORCID 0000-0003-4303-8116

Funding

Jiangsu Province Foundation BK20240296National Natural Science Foundation of China 82404173
6 · The paper itself

Abstract

Psoriasis is a common, chronic inflammatory skin disorder with a high prevalence across all age groups, imposing a substantial burden on both individuals and society. It is characterized by epidermal hyperplasia and infiltration of immune cells into the dermis. Within the psoriatic microenvironment, epidermal keratinocytes contribute to a self-amplifying inflammatory response through the generation of "feed-forward" inflammation. Contrary to the earlier view of keratinocytes as passive "victims" in psoriasis pathogenesis, growing evidence supports their role as "active drivers" of disease progression. Programmed cell death (PCD) in keratinocytes interacts dynamically with immune cells, cytokines, damage-associated molecular patterns (DAMPs), and other factors, forming a complex regulatory network. Multiple PCD-related molecules in keratinocytes have been identified, many of which hold promise as biomarkers or therapeutic targets. These molecules may inform the development of new diagnostic and treatment strategies for psoriasis. This review outlines the major PCD pathways in keratinocytes-apoptosis, necroptosis, ferroptosis, and pyroptosis-and examines their roles in psoriasis. We also summarize recent therapeutic advances that modulate keratinocyte cell death and discuss how these pathways shape the cutaneous immune microenvironment.

Indexed as

ApoptosisKeratinocytesPsoriasisAnimalsHumansNecroptosisPyroptosisSignal TransductionApoptosisEpidermisInflammatory skin diseasesNecroptosisPyroptosis

Identifiers

What Socratic 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 Socratic graph.