Evidence map›Paper›PMID 41805862›Full record

ReviewProtoplasma2026

Interplay of different signaling mechanisms in regulating programmed cell death during plant development and in response to stresses.

Rehman Sarwar, Ke-Ming Zhu, Wei Zhang, Yuanxue Liang, Xiao-Li Tan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Protoplasma, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

5 authors.

Rehman SarwarSchool of Life Sciences, Jiangsu University, Zhenjiang, China.
Ke-Ming ZhuSchool of Life Sciences, Jiangsu University, Zhenjiang, China.
Wei ZhangSchool of Life Sciences, Jiangsu University, Zhenjiang, China.
Yuanxue LiangSchool of Life Sciences, Jiangsu University, Zhenjiang, China.
Xiao-Li TanSchool of Life Sciences, Jiangsu University, Zhenjiang, China. xltan@ujs.edu.cn.

Funding

Jiangsu Provincial Key Research and Development Program BE2023342; BE2022340National Key Research and Development Program of China 2024YFD1200401National Natural Science Foundation of China 32472106
6 · The paper itself

Abstract

Programmed cell death (PCD) is a tightly controlled genetically regulated biological process, that controls morphogenic changes in any cell types during plant development or in response to environmental cues. Previously, significant progress has been made in identifying the key molecular players regulating the PCD process, how these components are integrated into context specific networks across developmental (dPCD) and environmentally induced PCD (ePCD) remains incompletely understood. This review summarizes the current understanding of PCD associated key molecular players, including calcium ions (Ca2+), reactive oxygen species (ROS), caspase-like proteases activity, transcriptional factors (TFs), and phytohormone signaling network and explicitly compares how their crosstalk orchestrate the initiation and execution of both dPCD and ePCD under biotic and abiotic stresses. A deeper mechanistic understanding of these interconnected signaling networks, and elucidating the crosstalk between development and stress induced PCD pathways might have significant implications in crop improvement as manipulating PCD processes can enhance crop disease resistance, optimize organ development and improve stress tolerance.

Indexed as

Abiotic stressApoptosisBiotic stressProgramed Cell Death (PCD)SenescenceVacuolar processing enzymes (VPEs)WRKY Binding Domain proteins (WRKYs)

Identifiers

PMID41805862

What OpenQuestion holds

Textmetadata
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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.