Evidence map›Paper›PMID 32875173›Full record

ReviewJACC. Basic to translational science2020

Autosis: A New Target to Prevent Cell Death.

Jihoon Nah, Daniela Zablocki, Junichi Sadoshima

Open access · goldAbstract readReview
In one paragraph

Review in JACC. Basic to translational science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

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  19. Molecular biology of the cell · 2024
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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

3 authors at 1 institution in 1 country.

Jihoon NahDepartment of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, New Jersey.
Daniela ZablockiDepartment of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, New Jersey.
Junichi SadoshimaDepartment of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, New Jersey.
Rutgers, The State University of New Jersey · US

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
Removal of damaged mitochondria by alternative autophagyR01HL138720 · NHLBI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI SADOSHIMA, JUNICHI · 2017 to 2024
$4.7M
GSK-3beta inhibits lipotoxicityR01HL144626 · NHLBI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI Junichi Sadoshima · 2019 to 2026
$3.0M
Vevo 3100 High Resolution Imaging SystemS10OD025238 · OD · RBHS-NEW JERSEY MEDICAL SCHOOL · PI VATNER, STEPHEN F · 2018 to 2018
$459k
NHLBI NIH HHS R01 HL091469NHLBI NIH HHS R01 HL112330NHLBI NIH HHS R01 HL138720NHLBI NIH HHS R01 HL144626NIH HHS S10 OD025238
6 · The paper itself

Abstract

Excessive autophagy induces a defined form of cell death called autosis, which is characterized by unique morphological features, including ballooning of perinuclear space and biochemical features, including sensitivity to cardiac glycosides. Autosis is observed during the late phase of reperfusion after a period of ischemia and contributes to myocardial injury. This review discusses unique features of autosis, the involvement of autosis in myocardial injury, and the molecular mechanism of autosis. Because autosis promotes myocardial injury under some conditions, a better understanding of autosis may lead to development of novel interventions to protect the heart against myocardial stress.

Indexed as

ATG, autophagy-relatedATPase, adenosine triphosphataseautophagic cell deathautophagic fluxautosisbeclin 1ER, endoplasmic reticulumHIV, human immunodeficiency virusI/R, ischemia-reperfusionLBR, lamin B receptorNa+,K+–adenosine triphosphatasePI3K, phosphatidylinositol 3 kinasePNS, perinuclear spacerubiconTat, transactivation of transcription

Identifiers

PMID32875173
PMCPMC7452304
OpenAlexW3080827788

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.