Evidence map›Paper›PMID 28366876›Full record

ReviewBiochimica et biophysica acta. Molecular basis of disease2017

Endothelial cell calpain as a critical modulator of angiogenesis.

Yixuan Zhang, Norika Mengchia Liu, Yongchen Wang, Ji Youn Youn, Hua Cai

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta. Molecular basis of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

31 citing papers in PubMed, 53 citations in OpenAlex.

  1. World journal of diabetes · 2025
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  14. Mechanosensitive channel Piezo1 is required for pulmonary artery smooth muscle cell proliferation.American journal of physiology. Lung cellular and molecular physiology · 2022
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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

5 authors at 1 institution in 1 country.

Yixuan ZhangDivision of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine at University of California Los Angeles (UCLA), CA 90095, USA; Division of Cardiology, Department Medicine, Cardiovascular Research Laboratories, David Geffen School of Medicine at University of California Los Angeles (UCLA), CA 90095, USA.
Norika Mengchia LiuDivision of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine at University of California Los Angeles (UCLA), CA 90095, USA; Division of Cardiology, Department Medicine, Cardiovascular Research Laboratories, David Geffen School of Medicine at University of California Los Angeles (UCLA), CA 90095, USA.
Yongchen WangDivision of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine at University of California Los Angeles (UCLA), CA 90095, USA; Division of Cardiology, Department Medicine, Cardiovascular Research Laboratories, David Geffen School of Medicine at University of California Los Angeles (UCLA), CA 90095, USA.
Ji Youn YounDivision of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine at University of California Los Angeles (UCLA), CA 90095, USA; Division of Cardiology, Department Medicine, Cardiovascular Research Laboratories, David Geffen School of Medicine at University of California Los Angeles (UCLA), CA 90095, USA.
Hua CaiDivision of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine at University of California Los Angeles (UCLA), CA 90095, USA; Division of Cardiology, Department Medicine, Cardiovascular Research Laboratories, David Geffen School of Medicine at University of California Los Angeles (UCLA), CA 90095, USA. Electronic address: hcai@mednet.ucla.edu.
University of California, Los Angeles · US

Funding

Angiotensin II Uncoupling of Enos in HypertensionR01HL077440 · NHLBI · UNIVERSITY OF CHICAGO · PI CAI, HUA LINDA · 2005 to 2019
$4.8M
NOXs, eNOS Uncoupling and Diabetic AtherogenesisR01HL088975 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CAI, HUA LINDA · 2010 to 2019
$4.5M
Mitochondrial pathways in NO induced cardioprotectionR01HL101228 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CAI, HUA LINDA, PING, PEIPEI · 2010 to 2013
$2.6M
Endothelium-Myocardium Interaction in Netrin-1 Induced CardioprotectionR01HL119968 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CAI, HUA LINDA · 2013 to 2017
$2.5M
Role of Vascular Oxidative Stress in ObesityR01HL108701 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CAI, HUA LINDA, HARRISON, DAVID G · 2012 to 2015
$1.9M
NHLBI NIH HHS R01 HL077440NHLBI NIH HHS R01 HL088975NHLBI NIH HHS R01 HL101228NHLBI NIH HHS R01 HL108701NHLBI NIH HHS R01 HL119968
6 · The paper itself

Abstract

Calpains are a family of calcium-dependent non-lysosomal cysteine proteases. In particular, calpains residing in the endothelial cells play important roles in angiogenesis. It has been shown that calpain activity can be increased in endothelial cells by growth factors, primarily vascular endothelial growth factor (VEGF). VEGF/VEGFR2 induces calpain 2 dependent activation of PI3K/AMPK/Akt/eNOS pathway, and consequent nitric oxide production and physiological angiogenesis. Under pathological conditions such as tumor angiogenesis, endothelial calpains can be activated by hypoxia. This review focuses on the molecular regulatory mechanisms of calpain activation, and the newly identified mechanistic roles and downstream signaling events of calpains in physiological angiogenesis, and in the conditions of pathological tumor angiogenesis and diabetic wound healing, as well as retinopathy and atherosclerosis that are also associated with an increase in calpain activity. Further discussed include the differential strategies of modulating angiogenesis through manipulating calpain expression/activity in different pathological settings. Targeted limitation of angiogenesis in cancer and targeted promotion of angiogenesis in diabetic wound healing via modulations of calpains and calpain-dependent signaling mechanisms are of significant translational potential. Emerging strategies of tissue-specific targeting, environment-dependent targeting, and genome-targeted editing may turn out to be effective regimens for targeted manipulation of angiogenesis through calpain pathways, for differential treatments including both attenuation of tumor angiogenesis and potentiation of diabetic angiogenesis.

Indexed as

AnimalsCalpainEndothelial CellsHumansNeovascularization, PathologicCalpainAngiogenesisAtherosclerosisCalpainDiabetic wound healingEndothelial cellseNOSRetinopathyShear stressTumor angiogenesisVEGF

Identifiers

PMID28366876
PMCPMC6511073
OpenAlexW2599539888

What Socratic 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 Socratic graph.