Evidence map›Paper›PMID 26807691›Full record

ArticleJournal of molecular and cellular cardiology2016

Increased fibroblast chymase production mediates procollagen autophagic digestion in volume overload.

Lianwu Fu, Chih-Chang Wei, Pamela C Powell, Wayne E Bradley, Sarfaraz Ahmad, Carlos M Ferrario, James F Collawn, Louis J Dell'Italia

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Heart Failure in Menopause: Treatment and New Approaches.International journal of molecular sciences · 2022
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  16. Chymase-dependent production of angiotensin II: an old enzyme in old hearts.American journal of physiology. Heart and circulatory physiology · 2017
    Article
  17. Review
  18. Intracrine angiotensin II functions originate from noncanonical pathways in the human heart.American journal of physiology. Heart and circulatory physiology · 2016
    Review
  19. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Lianwu FuBirmingham Veteran Affairs Medical Center, University of Alabama at Birmingham, Birmingham, AL, United States; Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL, United States.
Chih-Chang WeiBirmingham Veteran Affairs Medical Center, University of Alabama at Birmingham, Birmingham, AL, United States; Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, United States.
Pamela C PowellBirmingham Veteran Affairs Medical Center, University of Alabama at Birmingham, Birmingham, AL, United States.
Wayne E BradleyDivision of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, United States.
Sarfaraz AhmadDivision of Surgical Sciences, Wake Forest University School of Medicine, Winston-Salem, NC, United States.
Carlos M FerrarioDivision of Surgical Sciences, Wake Forest University School of Medicine, Winston-Salem, NC, United States.
James F CollawnDepartment of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL, United States.
Louis J Dell'ItaliaBirmingham Veteran Affairs Medical Center, University of Alabama at Birmingham, Birmingham, AL, United States; Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, United States; Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL, United States. Electronic address: louis.dellitalia@va.gov.
Birmingham VA Medical Center · USUniversity of Alabama at Birmingham · USWake Forest University · US

Funding

Vaso-Hormonal Mechanisms in HypertensionP01HL051952 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI GROBAN, LEANNE · 1994 to 2019
$34.8M
The Kallikrein/Kinin-Mast Cell Interaction in Volume OverloadI01BX001050 · VA · BIRMINGHAM VA MEDICAL CENTER · PI WEI, CHIH-CHANG KEVIN · 2011 to 2014
–
Pathophysiology of Extracellular Matrix and Desmin Breakdown in Volume Overload HeartI01BX003664 · VA · BIRMINGHAM VA MEDICAL CENTER · PI DELL'ITALIA, LOUIS J. · 2017 to 2020
–
The Chymase Angiotensin-(1-12) Axis in Heart DiseaseI01CX000993 · VA · BIRMINGHAM VA MEDICAL CENTER · PI DELL'ITALIA, LOUIS J. · 2014 to 2017
–
BLRD VA I01 BX001050BLRD VA I01 BX003664CSRD VA I01 CX000993NHLBI NIH HHS P01 HL051952
6 · The paper itself

Abstract

backgroundPrevious work has identified mast cells as the major source of chymase largely associated with a profibrotic phenotype. We recently reported increased fibroblast autophagic procollagen degradation in a rat model of pure volume overload (VO). Here we demonstrate a connection between increased fibroblast chymase production and autophagic digestion of procollagen in the pure VO of aortocaval fistula (ACF) in the rat. METHODS AND

resultsIsolated LV fibroblasts taken from 4 and 12week ACF Sprague-Dawley rats have significant increases in chymase mRNA and chymase activity. Increased intracellular chymase protein is documented by immunocytochemistry in the ACF fibroblasts compared to cells obtained from age-matched sham rats. To implicate VO as a stimulus for chymase production, we show that isolated adult rat LV fibroblasts subjected to 24h of 20% cyclical stretch induces chymase mRNA and protein production. Exogenous chymase treatment of control isolated adult cardiac fibroblasts demonstrates that chymase is internalized through a dynamin-dependent mechanism. Chymase treatment leads to an increased formation of autophagic vacuoles, LC3-II production, autophagic flux, resulting in increased procollagen degradation. Chymase inhibitor treatment reduces cyclical stretch-induced autophagy in isolated cardiac fibroblasts, demonstrating chymase's role in autophagy induction.

conclusionIn a pure VO model, chymase produced in adult cardiac fibroblasts leads to autophagic degradation of newly synthesized intracellular procollagen I, suggesting a new role of chymase in extracellular matrix degradation.

Indexed as

AnimalsAortaArterio-Arterial FistulaAutophagyChymasesExtracellular MatrixFibroblastsHeart FailureHumansMast CellsMyocardiumPhagosomesProcollagenProteolysisRatsRNA, MessengerChymasesProcollagenRNA, MessengerAutophagyCardiac fibroblastChymaseIntracellular procollagenVolume overload

Identifiers

PMID26807691
PMCPMC5198899
OpenAlexW2251421794

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.