Cardiac fibroblast‐specific p38α MAP kinase promotes cardiac hypertrophy via a putative paracrine interleukin‐6 signaling mechanism-Reference-Cited by-同舟云学术

Cardiac fibroblast‐specific p38α MAP kinase promotes cardiac hypertrophy via a putative paracrine interleukin‐6 signaling mechanism

Published:2018-03-30 Issue:9 Volume:32 Page:4941-4954
ISSN:0892-6638
Container-title:The FASEB Journal
language:en
Short-container-title:FASEB j.

Author:

Bageghni Sumia A.¹,Hemmings Karen E.¹,Zava Ngonidzashe¹,Denton Christopher P.²,Porter Karen E.¹,Ainscough Justin F. X.¹,Drinkhill Mark J.¹,Turner Neil A.¹

Affiliation:

1. Leeds Institute of Cardiovascular and Metabolic MedicineSchool of MedicineUniversity of LeedsLeedsUnited Kingdom

2. Centre for RheumatologyDivision of MedicineUniversity College LondonLondonUnited Kingdom

Funder

British Heart Foundation

Publisher

Wiley

Subject

Genetics,Molecular Biology,Biochemistry,Biotechnology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1096/fj.201701455RR

Reference73 articles.

1. Therapeutic regulation of cardiac fibroblast function: targeting stress-activated protein kinase pathways

2. p38 MAP kinases in the heart

3. The p38 mitogen-activated protein kinase pathway—A potential target for intervention in infarction, hypertrophy, and heart failure

4. The case for inhibiting p38 mitogen-activated protein kinase in heart failure

5. Decreased p38 MAPK Activity in End-Stage Failing Human Myocardium: p38 MAPK α is the Predominant Isoform Expressed in Human Heart

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