Evidence map›Paper›PMID 32384150›Full record

ArticleCardiovascular research2021

Targeting mitochondrial fission as a potential therapeutic for abdominal aortic aneurysm.

Hannah A Cooper, Stephanie Cicalese, Kyle J Preston, Tatsuo Kawai, Keisuke Okuno, Eric T Choi, Shingo Kasahara, Haruhito A Uchida, Nozomu Otaka, Rosario Scalia and 2 more

Open access · greenAbstract read
In one paragraph

Article in Cardiovascular research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
7.6field-weighted citation impact, top 2% 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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

  1. Pooled it
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  3. Review
  4. Review
  5. Leptin Aggravates Thoracic Aortic Dissection Through Impairment of Energy Metabolism in Nrip2Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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  16. Mitochondrial fission inhibition protects against hypertension induced by angiotensin II.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 2 countries.

Hannah A CooperCardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Stephanie CicaleseCardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Kyle J PrestonCardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Tatsuo KawaiCardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Keisuke OkunoCardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Eric T ChoiDepartment of Surgery, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Shingo KasaharaDepartment of Cardiovascular Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan.
Haruhito A UchidaDepartment of Chronic Kidney Disease and Cardiovascular Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan.
Nozomu OtakaDepartment of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan.
Rosario ScaliaCardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Victor RizzoCardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Satoru EguchiCardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Temple University · USOkayama University · JP

Funding

Inflammatory Responses of The Visceral Adipose Tissue MicrocirculationR01DK111042 · NIDDK · TEMPLE UNIV OF THE COMMONWEALTH · PI EGUCHI, SATORU, SCALIA, ROSARIO G · 2017 to 2020
$2.3M
EGF-ADAM17 axis in the pathophysiology of intracranial aneurysmR01NS109382 · NINDS · ST. JOSEPH'S HOSPITAL AND MEDICAL CENTER · PI EGUCHI, SATORU, HASHIMOTO, TOMOKI · 2019 to 2023
$2.2M
Mechanism of Hypertensive Vascular Remodeling and End-Organ DamageR01HL133248 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI EGUCHI, SATORU · 2016 to 2019
$1.8M
Vascular signal as a therapeutic target for abdominal aortic aneurysmR01HL128324 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI EGUCHI, SATORU, RIZZO, VICTOR J. · 2015 to 2018
$1.6M
Mitochondrial fission mediates hypertensive vascular remodelingF30HL146006 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI COOPER, HANNAH ABIGAIL · 2019 to 2020
$82k
NHLBI NIH HHS F30 HL146006NHLBI NIH HHS R01 HL128324NHLBI NIH HHS R01 HL133248NIDDK NIH HHS R01 DK111042NINDS NIH HHS R01 NS109382
6 · The paper itself

Abstract

aimsAngiotensin II (AngII) is a potential contributor to the development of abdominal aortic aneurysm (AAA). In aortic vascular smooth muscle cells (VSMCs), exposure to AngII induces mitochondrial fission via dynamin-related protein 1 (Drp1). However, pathophysiological relevance of mitochondrial morphology in AngII-associated AAA remains unexplored. Here, we tested the hypothesis that mitochondrial fission is involved in the development of AAA. METHODS AND

resultsImmunohistochemistry was performed on human AAA samples and revealed enhanced expression of Drp1. In C57BL6 mice treated with AngII plus β-aminopropionitrile, AAA tissue also showed an increase in Drp1 expression. A mitochondrial fission inhibitor, mdivi1, attenuated AAA size, associated aortic pathology, Drp1 protein induction, and mitochondrial fission but not hypertension in these mice. Moreover, western-blot analysis showed that induction of matrix metalloproteinase-2, which precedes the development of AAA, was blocked by mdivi1. Mdivi1 also reduced the development of AAA in apolipoprotein E-deficient mice infused with AngII. As with mdivi1, Drp1+/- mice treated with AngII plus β-aminopropionitrile showed a decrease in AAA compared to control Drp1+/+ mice. In abdominal aortic VSMCs, AngII induced phosphorylation of Drp1 and mitochondrial fission, the latter of which was attenuated with Drp1 silencing as well as mdivi1. AngII also induced vascular cell adhesion molecule-1 expression and enhanced leucocyte adhesion and mitochondrial oxygen consumption in smooth muscle cells, which were attenuated with mdivi1.

conclusionThese data indicate that Drp1 and mitochondrial fission play salient roles in AAA development, which likely involves mitochondrial dysfunction and inflammatory activation of VSMCs.

Indexed as

AminopropionitrileAngiotensin IIAnimalsAnti-Inflammatory AgentsAorta, AbdominalAortic Aneurysm, AbdominalCase-Control StudiesCell AdhesionCells, CulturedDisease Models, AnimalDynaminsHumansLeukocytesMaleMiceMice, Inbred C57BL3-(2,4-dichloro-5-methoxyphenyl)-2-sulfanyl-4(3H)-quinazolinoneAminopropionitrileAngiotensin IIAnti-Inflammatory AgentsDNM1L protein, humanDnm1l protein, mouseDynaminsQuinazolinonesAbdominal aortic aneurysmInflammationMitochondriaSenescenceVascular smooth muscle cell

Identifiers

PMID32384150
PMCPMC7898955
OpenAlexW3022481902

What OpenQuestion holds

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Registered trials

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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.