Evidence map›Paper›PMID 36337896›Full record

ReviewFrontiers in cardiovascular medicine2022

Mitochondria-associated endoplasmic reticulum membranes and cardiac hypertrophy: Molecular mechanisms and therapeutic targets.

Yi Luan, Yage Jin, Pengjie Zhang, Hongqiang Li, Yang Yang

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
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

12 citing papers in PubMed, 20 citations in OpenAlex.

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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 at 1 institution in 1 country.

Yi LuanClinical Systems Biology Research Laboratories, Translational Medicine Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yage JinDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Pengjie ZhangDepartment of Ultrasound, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Hongqiang LiDepartment of Thyroid Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yang YangClinical Systems Biology Research Laboratories, Translational Medicine Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac hypertrophy has been shown to compensate for cardiac performance and improve ventricular wall tension as well as oxygen consumption. This compensatory response results in several heart diseases, which include ischemia disease, hypertension, heart failure, and valvular disease. Although the pathogenesis of cardiac hypertrophy remains complicated, previous data show that dysfunction of the mitochondria and endoplasmic reticulum (ER) mediates the progression of cardiac hypertrophy. The interaction between the mitochondria and ER is mediated by mitochondria-associated ER membranes (MAMs), which play an important role in the pathology of cardiac hypertrophy. The function of MAMs has mainly been associated with calcium transfer, lipid synthesis, autophagy, and reactive oxygen species (ROS). In this review, we discuss key MAMs-associated proteins and their functions in cardiovascular system and define their roles in the progression of cardiac hypertrophy. In addition, we demonstrate that MAMs is a potential therapeutic target in the treatment of cardiac hypertrophy.

Indexed as

cardiac hypertrophycardiovascular systemMAMs-associated proteinsmitochondria-associated ER membranes (MAMs)therapeutic targets

Identifiers

PMID36337896
PMCPMC9630933
OpenAlexW4306945870

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.