Evidence map›Paper›PMID 31109279›Full record

ReviewCurrent topics in medicinal chemistry2019

Unfolded Protein Response as a Therapeutic Target in Cardiovascular Disease.

Guangyu Zhang, Xiaoding Wang, Thomas G Gillette, Yingfeng Deng, Zhao V Wang

Abstract readReview
In one paragraph

Review in Current topics in medicinal chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 40 citations in OpenAlex.

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  15. Adipocyte-specific deletion of HuR induces spontaneous cardiac hypertrophy and fibrosis.American journal of physiology. Heart and circulatory physiology · 2021
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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.

Guangyu ZhangDivision of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, United States.
Xiaoding WangDivision of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, United States.
Thomas G GilletteDivision of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, United States.
Yingfeng DengTouchstone Diabetes Center, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, United States.
Zhao V WangDivision of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, United States.
The University of Texas Southwestern Medical Center · US

Funding

Role of the Xbp1s/GFAT1 axis in pathological cardiac remodellingR01HL137723 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI WANG, ZHAO · 2017 to 2025
$4.3M
NHLBI NIH HHS R01 HL137723
6 · The paper itself

Abstract

Cardiovascular disease is the leading cause of death worldwide. Despite overwhelming socioeconomic impact and mounting clinical needs, our understanding of the underlying pathophysiology remains incomplete. Multiple forms of cardiovascular disease involve an acute or chronic disturbance in cardiac myocytes, which may lead to potent activation of the Unfolded Protein Response (UPR), a cellular adaptive reaction to accommodate protein-folding stress. Accumulation of unfolded or misfolded proteins in the Endoplasmic Reticulum (ER) elicits three signaling branches of the UPR, which otherwise remain quiescent. This ER stress response then transiently suppresses global protein translation, augments production of protein-folding chaperones, and enhances ER-associated protein degradation, with an aim to restore cellular homeostasis. Ample evidence has established that the UPR is strongly induced in heart disease. Recently, the mechanisms of action and multiple pharmacological means to favorably modulate the UPR are emerging to curb the initiation and progression of cardiovascular disease. Here, we review the current understanding of the UPR in cardiovascular disease and discuss existing therapeutic explorations and future directions.

Indexed as

AnimalsCardiovascular AgentsCardiovascular DiseasesEndoplasmic ReticulumEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressHumansUnfolded Protein ResponseCardiovascular AgentsEndoplasmic Reticulum Chaperone BiPHSPA5 protein, humanATF6cardiovascular diseaseendoplasmic reticulumGRP78IRE1ischemic heart diseasepathological cardiac remodeling.PERKUnfolded protein responseXBP1s

Identifiers

PMID31109279
PMCPMC7024549
OpenAlexW2945884340

What OpenQuestion holds

Textmetadata
LicenceTDM
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.