Evidence map›Paper›PMID 41075142›Full record

ReviewCell biochemistry and biophysics2026

EVA1A-Mediated Signaling Networks in Physiological and Pathological Contexts: Dual Roles in Autophagy and Apoptosis.

Chenglin Zhu, Qi Zhang, Hao Fan, Bohong Guo, Honggang Wang

Abstract readReview
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In one paragraph

Review in Cell biochemistry and biophysics, 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.

Chenglin ZhuHenan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, Henan, China.
Qi ZhangHenan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, Henan, China.
Hao FanHenan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, Henan, China.
Bohong GuoHenan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, Henan, China.
Honggang WangHenan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, Henan, China. whg197167@vip.henu.edu.cn.

Funding

he grants from the key scientific and technological projects in Henan Province, China 252102310124
6 · The paper itself

Abstract

Eva-1 homolog A (EVA1A) is a transmembrane protein localized on the endoplasmic reticulum and lysosomes. As a key regulator of autophagy and apoptosis, EVA1A regulates neurogenesis, cardioprotection, tumor suppression, and metabolic homeostasis. In this review, we synthesize the multifaceted signaling networks through which EVA1A modulates physiological and pathological processes. These include the PI3K/AKT/mTOR axis (governing neural stem cell maintenance and hepatocellular carcinoma drug resistance), LKB1/AMPK/mTOR pathway (mediating mitochondrial quality control in cardiac injury), mTOR/RPS6KB1 signaling (suppressing glioblastoma proliferation via autophagy-apoptosis crosstalk), and the Hippo-YAP/TAZ cascade (influencing epithelial-mesenchymal transition in thyroid cancer). Crucially, EVA1A exhibits context-dependent dual roles: promoting autophagic flux for homeostasis or triggering apoptosis under stress. Most of these findings are derived from preclinical studies using cell lines and animal models, with limited validation in human tissues or clinical cohorts.We emphasize EVA1A paradoxical effects in cancers, where EVA1A acts as either a tumor suppressor or a modulator of therapy resistance, depending on the tissue-specific microenvironment. Furthermore, EVA1A’s involvement in neurodegenerative and metabolic diseases, such as Alzheimer’s, Parkinson’s, obesity, and diabetes, remains underexplored, despite its relevance to autophagy and inflammation. Understanding the spatiotemporal dynamics of EVA1A interactions with autophagy-related complexes (such as ATG16L1/ATG5/ATG12) and stress-responsive pathways is important to explore its therapeutic potential. However, EVA1A-targeted therapy is still in the early discovery phase, with no current clinical applications.Future studies should focus on the molecular crosstalk between EVA1A-mediated autophagy and metabolic/inflammatory pathways, aiming to facilitate EVA1A-targeted therapeutic development.

Indexed as

ApoptosisAutophagyMembrane ProteinsSignal TransductionAnimalsHumansNeoplasmsNeurodegenerative DiseasesEVA1A protein, humanMembrane ProteinsApoptosisAutophagyCancerEVA1ATherapeutic target

Identifiers

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Registered trials

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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.