Evidence map›Paper›PMID 36717246›Full record

ArticleLife science alliance2023

Cardiac Plin5 interacts with SERCA2 and promotes calcium handling and cardiomyocyte contractility.

Mathieu Cinato, Ismena Mardani, Azra Miljanovic, Christina Drevinge, Marion Laudette, Entela Bollano, Marcus Henricsson, Johan Tolö, Marcos Bauza Thorbrügge, Max Levin and 7 more

Open access · goldAbstract read
In one paragraph

Article in Life science alliance, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 11 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

17 authors at 3 institutions in 2 countries.

Mathieu CinatoDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, Sahlgrenska Academy at University of Gothenburgand Sahlgrenska University Hospital, Gothenburg, Sweden.ORCID https://orcid.org/0000-0002-8490-4335
Ismena MardaniDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, Sahlgrenska Academy at University of Gothenburgand Sahlgrenska University Hospital, Gothenburg, Sweden.
Azra MiljanovicDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, Sahlgrenska Academy at University of Gothenburgand Sahlgrenska University Hospital, Gothenburg, Sweden.ORCID https://orcid.org/0000-0003-0290-5711
Christina DrevingeDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, Sahlgrenska Academy at University of Gothenburgand Sahlgrenska University Hospital, Gothenburg, Sweden.
Marion LaudetteDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, Sahlgrenska Academy at University of Gothenburgand Sahlgrenska University Hospital, Gothenburg, Sweden.ORCID https://orcid.org/0000-0002-3431-9103
Entela BollanoDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, Sahlgrenska Academy at University of Gothenburgand Sahlgrenska University Hospital, Gothenburg, Sweden.
Marcus HenricssonDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, Sahlgrenska Academy at University of Gothenburgand Sahlgrenska University Hospital, Gothenburg, Sweden.ORCID https://orcid.org/0000-0002-4202-0339
Johan TolöDepartment of Physiology/Metabolic Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.ORCID https://orcid.org/0000-0001-9648-4721
Marcos Bauza ThorbrüggeDepartment of Physiology/Metabolic Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.ORCID https://orcid.org/0000-0002-2147-9386
Max LevinDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, Sahlgrenska Academy at University of Gothenburgand Sahlgrenska University Hospital, Gothenburg, Sweden malin.levin@wlab.gu.se.ORCID https://orcid.org/0000-0001-9676-5582
Malin LindbomDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, Sahlgrenska Academy at University of Gothenburgand Sahlgrenska University Hospital, Gothenburg, Sweden.
Muhammad ArifLaboratory of Cardiovascular Physiology and Tissue Injury, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.ORCID https://orcid.org/0000-0003-2261-0881
Pal PacherLaboratory of Cardiovascular Physiology and Tissue Injury, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.
Linda AnderssonDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, Sahlgrenska Academy at University of Gothenburgand Sahlgrenska University Hospital, Gothenburg, Sweden.
Charlotta S OlofssonDepartment of Physiology/Metabolic Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
Jan BorénDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, Sahlgrenska Academy at University of Gothenburgand Sahlgrenska University Hospital, Gothenburg, Sweden.
Malin C LevinDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, Sahlgrenska Academy at University of Gothenburgand Sahlgrenska University Hospital, Gothenburg, Sweden malin.levin@wlab.gu.se.ORCID https://orcid.org/0000-0003-1069-5275
Sahlgrenska University Hospital · SEUniversity of Gothenburg · SENational Institutes of Health · US

Funding

Mechanism of oxidative/nitrosative stress and inflammation-induced tissue injuryZIAAA000375 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI PACHER, PAL · 2009 to 2025
$27.8M
6 · The paper itself

Abstract

The adult heart develops hypertrophy to reduce ventricular wall stress and maintain cardiac function in response to an increased workload. Although pathological hypertrophy generally progresses to heart failure, physiological hypertrophy may be cardioprotective. Cardiac-specific overexpression of the lipid-droplet protein perilipin 5 (Plin5) promotes cardiac hypertrophy, but it is unclear whether this response is beneficial. We analyzed RNA-sequencing data from human left ventricle and showed that cardiac

Indexed as

Calcium SignalingHeart FailureMyocytes, CardiacPerilipin-5AnimalsCalciumCardiomegalyHumansMiceSarcoplasmic Reticulum Calcium-Transporting ATPasesAtp2a2 protein, mouseCalciumPerilipin-5Plin5 protein, mouseSarcoplasmic Reticulum Calcium-Transporting ATPases

Identifiers

PMID36717246
PMCPMC9887753
OpenAlexW4318499623

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.