Evidence map›Paper›PMID 40128893›Full record

ArticleJournal of translational medicine2025

Mfn2 regulates calcium homeostasis and suppresses PASMCs proliferation via interaction with IP3R3 to mitigate pulmonary arterial hypertension.

Rui Wang, Jie Wang, Jing Yu, Zhiqiang Li, Minfang Zhang, Yuhu Chen, Fen Liu, Dongmei Jiang, Jingfei Guo, Xiaomei Li and 1 more

Abstract read
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Effects ofNutrients · 2025
    Trial
  2. Review
  3. Review
  4. Mitochondrial Calcium Signaling in Hepatocyte Health and Disease.Cold Spring Harbor perspectives in biology · 2026
    Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. 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

11 authors.

Rui Wang *Department of General Medicine, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, China.
Jie Wang *Department of Pharmacy, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, China.
Jing YuCollege of Pharmacy, Xinjiang Medical University, Urumqi, 830011, China.
Zhiqiang LiAnimal Laboratory Center, Xinjiang Medical University, Urumqi, 830011, China.
Minfang ZhangElectron Microscope Lab, Xinjiang Medical University, Urumqi, 830011, China.
Yuhu ChenDepartment of General Surgery, Lingcheng District People's Hospital, Dezhou, 253500, China.
Fen LiuA State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, China.
Dongmei JiangDepartment of General Medicine, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, China.
Jingfei GuoDepartment of General Medicine, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, China.
Xiaomei LiDepartment of Cardiology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, China. lixm505@163.com.
Yun WuDepartment of General Medicine, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, China. wuyun8009@163.com.

Funding

National Natural Science Foundation of China 82260081the Xinjiang Uygur Autonomous Region Youth Science and Technology Top Talent Project-Youth Science and Technology Innovation Talent Training 2022TSYCCX0034
6 · The paper itself

Abstract

backgroundPulmonary arterial hypertension (PAH) is a chronic disorder characterized by the excessive proliferation of pulmonary arterial smooth muscle cells (PASMCs). Recent studies indicate that Mitochondrial fusion protein 2 (Mfn2) maintains intracellular calcium (Ca

methodsThis study explored the roles of Mfn2 and IP3R3 in PAH progression by assessing their expression in lung tissues of a monocrotaline (MCT)-induced PAH rat model. Immunoprecipitation assays were performed to confirm the interaction between Mfn2 and IP3R3. PASMCs were treated with either silenced or overexpressed Mfn2 and exposed to TNF-ɑ to observe effects on ER stress, IP3R3 expression, mitochondrial Ca

resultsMfn2 expression was significantly down-regulated in the MCT-induced PAH rat model. Inhibition of ER stress upregulated Mfn2 expression, downregulated IP3R3 expression, increased mitochondrial Ca

conclusionsMfn2 mediates mitochondrial Ca

Indexed as

CalciumGTP PhosphohydrolasesHomeostasisInositol 1,4,5-Trisphosphate ReceptorsMitochondrial ProteinsMyocytes, Smooth MusclePulmonary Arterial HypertensionPulmonary ArteryAnimalsCell ProliferationEndoplasmic Reticulum StressMaleMitochondriaProtein BindingRatsRats, Sprague-DawleyCalciumGTP PhosphohydrolasesInositol 1,4,5-Trisphosphate ReceptorsMfn2 protein, ratMitochondrial ProteinsCa2+ homeostasisEndoplasmic reticulum stressMfn2 interact with IP3R3Mitochondrial autophagyPulmonary artery hypertension

Identifiers

PMID40128893
PMCPMC11934582

What OpenQuestion holds

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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.