Evidence map›Paper›PMID 35597275›Full record

ReviewJournal of molecular and cellular cardiology2022

Necroptosis in heart disease: Molecular mechanisms and therapeutic implications.

Xiaoyun Guo, Yi Chen, Qinghang Liu

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
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  5. PPP1R3G-RIPK1-ZBP1 axis activates early-stage apoptosis and late-stage necroptosis to promote doxorubicin-induced cardiotoxicity.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  13. Molecular mechanisms and intervention approaches of heart failure (Review).International journal of molecular medicine · 2025
    Review
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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.

Xiaoyun GuoDepartment of Physiology and Biophysics, University of Washington, Seattle, WA, USA.
Yi ChenDepartment of Physiology and Biophysics, University of Washington, Seattle, WA, USA.
Qinghang LiuDepartment of Physiology and Biophysics, University of Washington, Seattle, WA, USA. Electronic address: qcliu@u.washington.edu.
University of Washington · US

Funding

A K63-Ubiquitination Dependent Necroptosis Signaling Network in the HeartR01HL155035 · NHLBI · UNIVERSITY OF WASHINGTON · PI LIU, QINGHANG · 2021 to 2025
$1.9M
The Deubiquitinase CYLD Controls Multiple Cell Death Pathways in the HeartR01HL160767 · NHLBI · UNIVERSITY OF WASHINGTON · PI LIU, QINGHANG · 2022 to 2025
$1.6M
NHLBI NIH HHS R01 HL155035NHLBI NIH HHS R01 HL160767
6 · The paper itself

Abstract

Cell death is a crucial event underlying cardiac ischemic injury, pathological remodeling, and heart failure. Unlike apoptosis, necrosis had long been regarded as a passive and unregulated process. However, recent studies demonstrate that a significant subset of necrotic cell death is actively mediated through regulated pathways - a process known as "regulated necrosis". As a form of regulated necrosis, necroptosis is mediated by death receptors and executed through the activation of receptor interacting protein kinase 3 (RIPK3) and its downstream substrate mixed lineage kinase-like domain (MLKL). Recent studies have provided compelling evidence that necroptosis plays an important role in myocardial homeostasis, ischemic injury, pathological remodeling, and heart failure. Moreover, it has been shown that genetic and pharmacological manipulations of the necroptosis signaling pathway elicit cardioprotective effects. Important progress has also been made regarding the molecular mechanisms that regulate necroptotic cell death in vitro and in vivo. In this review, we discuss molecular and cellular mechanisms of necroptosis, potential crosstalk between necroptosis and other cell death pathways, functional implications of necroptosis in heart disease, and new therapeutic strategies that target necroptosis signaling.

Indexed as

Heart DiseasesHeart FailureApoptosisHumansNecroptosisNecrosisProtein KinasesProtein KinasesApoptosisHeart failureMyocardial infarctionNecroptosisNecrosis

Identifiers

PMID35597275
PMCPMC9636888
OpenAlexW4280584556

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.