Evidence map›Paper›PMID 29420210›Full record

ReviewCirculation research2018

New Insights Into the Role of mTOR Signaling in the Cardiovascular System.

Sebastiano Sciarretta, Maurizio Forte, Giacomo Frati, Junichi Sadoshima

Open access · greenAbstract readReview
In one paragraph

Review in Circulation research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 291 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
291citing papers in PubMed, 1 pooled it
19.8field-weighted citation impact, top 1% 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

291 citing papers in PubMed, 1 synthesis or guideline pooled it, 469 citations in OpenAlex.

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  12. RRAGD p.(Ser76Leu) Variant Causes Dysregulated Expression of Muscle Development and Cytoskeleton Genes in Cardiomyocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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231 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Sebastiano SciarrettaFrom the Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy (S.S., G.F.); Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy (S.S., M.F., G.F.); and Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark (J.S.).
Maurizio ForteFrom the Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy (S.S., G.F.); Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy (S.S., M.F., G.F.); and Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark (J.S.).
Giacomo FratiFrom the Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy (S.S., G.F.); Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy (S.S., M.F., G.F.); and Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark (J.S.).
Junichi SadoshimaFrom the Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy (S.S., G.F.); Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy (S.S., M.F., G.F.); and Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark (J.S.). sadoshju@njms.rutgers.edu.
Istituto Neurologico Mediterraneo · ITSapienza University of Rome · IT

Funding

Cysteine oxidation in the heartR01HL091469 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI Junichi Sadoshima · 2008 to 2026
$9.4M
The Role of Serine Signaling in Compensatory Cardiac HypertrophyR01HL112330 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI Junichi Sadoshima · 2012 to 2026
$7.5M
The Role of Thioredoxin in the Aging HeartR01AG023039 · NIA · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SADOSHIMA, JUNICHI · 2004 to 2018
$5.8M
Regulation of myocardial growth and death by GSK-3R01HL067724 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SADOSHIMA, JUNICHI · 2000 to 2018
$5.1M
Removal of damaged mitochondria by alternative autophagyR01HL138720 · NHLBI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI SADOSHIMA, JUNICHI · 2017 to 2024
$4.7M
Regulation of myocardial growth and death by autophagyR01HL102738 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SADOSHIMA, JUNICHI · 2010 to 2014
$2.5M
NHLBI NIH HHS R01 HL067724NHLBI NIH HHS R01 HL091469NHLBI NIH HHS R01 HL102738NHLBI NIH HHS R01 HL112330NHLBI NIH HHS R01 HL138720NIA NIH HHS R01 AG023039
6 · The paper itself

Abstract

The mTOR (mechanistic target of rapamycin) is a master regulator of several crucial cellular processes, including protein synthesis, cellular growth, proliferation, autophagy, lysosomal function, and cell metabolism. mTOR interacts with specific adaptor proteins to form 2 multiprotein complexes, called mTORC1 (mTOR complex 1) and mTORC2 (mTOR complex 2). In the cardiovascular system, the mTOR pathway regulates both physiological and pathological processes in the heart. It is needed for embryonic cardiovascular development and for maintaining cardiac homeostasis in postnatal life. Studies involving mTOR loss-of-function models revealed that mTORC1 activation is indispensable for the development of adaptive cardiac hypertrophy in response to mechanical overload. mTORC2 is also required for normal cardiac physiology and ensures cardiomyocyte survival in response to pressure overload. However, partial genetic or pharmacological inhibition of mTORC1 reduces cardiac remodeling and heart failure in response to pressure overload and chronic myocardial infarction. In addition, mTORC1 blockade reduces cardiac derangements induced by genetic and metabolic disorders and has been reported to extend life span in mice. These studies suggest that pharmacological targeting of mTOR may represent a therapeutic strategy to confer cardioprotection, although clinical evidence in support of this notion is still scarce. This review summarizes and discusses the new evidence on the pathophysiological role of mTOR signaling in the cardiovascular system.

Indexed as

Cardiovascular Physiological PhenomenaSignal TransductionAdaptation, PhysiologicalAnimalsAutophagyCardiomegalyCell SurvivalEnergy MetabolismGene Expression RegulationHeart DiseasesHumansHypoxiaLipid MetabolismMammalsMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2Mechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2TOR Serine-Threonine Kinasesautophagycardiovascular diseaseshearthypertrophymice

Identifiers

PMID29420210
PMCPMC6398933
OpenAlexW2789055329

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.