Evidence map›Paper›PMID 42909985›Full record

ReviewFrontiers in immunology2026

Endoplasmic reticulum-mitochondria contact sites in benign prostatic hyperplasia: evidence integration and mechanistic hypotheses.

Lei Liu, Minhao Fu, Zhenting Wang

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in immunology, 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

3 authors.

Lei LiuHaikou Research Institute of Xiangya School of Medicine, Central South University, Haikou, China.
Minhao FuHaikou Research Institute of Xiangya School of Medicine, Central South University, Haikou, China.
Zhenting WangHaikou Research Institute of Xiangya School of Medicine, Central South University, Haikou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Benign prostatic hyperplasia (BPH) is a common chronic and progressive disease in ageing men. Its pathobiology involves androgen-signaling remodeling, chronic inflammation, oxidative stress, metabolic disturbance, and dysregulated cell fate control; however, the organelle-level communication that connects these processes remains insufficiently defined. Endoplasmic reticulum (ER)-mitochondria contact sites, commonly referred to as mitochondria-associated membranes (MAMs), are dynamic membrane contact platforms that coordinate ER stress with mitochondrial homeostasis. Through the regulation of Ca²

Indexed as

Endoplasmic ReticulumMitochondriaProstatic HyperplasiaAnimalsEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressHumansMaleMitochondria Associated MembranesMitochondrial DynamicsReactive Oxygen SpeciesSignal TransductionEndoplasmic Reticulum Chaperone BiPHSPA5 protein, humanReactive Oxygen Speciesageingbenign prostatic hyperplasiaendoplasmic reticulum stressinflammationmitochondria-associated membranesmitochondrial dysfunctionoxidative stress

Identifiers

PMID42909985
PMCPMC13684870

What OpenQuestion 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 OpenQuestion graph.