Evidence map›Paper›PMID 41608412›Full record

ReviewFrontiers in pharmacology2026

HtrA2/Omi: potential therapeutic targets for neurodegenerative diseases.

Liting Xu, Min Zeng

Abstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

2 authors.

Liting XuDepartment of Nephrology, People's Hospital of Longhua, Shenzhen, China.
Min ZengDepartment of Nephrology, People's Hospital of Longhua, Shenzhen, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High temperature requirement protein A2 (HtrA2/Omi), a key regulator of mitochondrial quality control, plays a pivotal role in determining cell fate through its subcellular localization, whether mitochondrial or cytosolic. Growing evidence links the absence or dysfunction of HtrA2 to the pathogenesis of neurodegenerative diseases. This review examines the structure and function of HtrA2, highlights its transcriptional regulators, explores its involvement in neurodegeneration, and outlines the currently identified agonists and inhibitors, offering new insights for developing HtrA2/Omi as a potential therapeutic target for neurodegenerative disorders.

Indexed as

apoptosisHtrA2mitochondrianeurodegenerative diseasesUCF-101

Identifiers

PMID41608412
PMCPMC12835204

What OpenQuestion holds

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LicenceCC BY
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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.