Zobrazeno 1 - 10
of 13
pro vyhledávání: '"Nehal J, Patel"'
Autor:
Drew M. Nassal, Rebecca Shaheen, Nehal J. Patel, Jane Yu, Nick Leahy, Dimitra Bibidakis, Narasimham L. Parinandi, Thomas J. Hund
Publikováno v:
Cells, Vol 12, Iss 5, p 748 (2023)
Cardiac fibroblasts (CFs) maintain the fibrous extracellular matrix (ECM) that supports proper cardiac function. Cardiac injury induces a transition in the activity of CFs to promote cardiac fibrosis. CFs play a critical role in sensing local injury
Externí odkaz:
https://doaj.org/article/a29e01bbb1b5463981044fe26df50d80
Autor:
Drew M, Nassal, Nehal J, Patel, Sathya D, Unudurthi, Rebecca, Shaheen, Jane, Yu, Peter J, Mohler, Thomas J, Hund
Publikováno v:
The Journal of Biological Chemistry
Fibrosis is a pronounced feature of heart disease and the result of dysregulated activation of resident cardiac fibroblasts (CFs). Recent work identified stress-induced degradation of the cytoskeletal protein βIV-spectrin as an important step in CF
Publikováno v:
Expert Opin Ther Targets
Introduction: Cardiac fibrosis contributes to the development of cardiovascular disease (CVD) and arrhythmia. Cardiac fibroblasts (CFs) are collagen-producing cells that regulate extracellular matrix (ECM) homeostasis. A complex signaling network has
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::91cfede265ed21365696b5f4b4287e05
Autor:
Amara Greer-Short, Thomas J. Hund, Peter J. Mohler, Drew M. Nassal, Tony Satroplus, Taylor Howard, Nehal J. Patel
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 315:H794-H801
The mechanisms underlying Ca2+/calmodulin-dependent protein kinase II (CaMKII)-induced arrhythmias in ischemia-reperfusion (I/R) are not fully understood. We tested the hypothesis that CaMKII increases late Na+current ( INa,L) via phosphorylation of
Publikováno v:
Expert Review of Cardiovascular Therapy. 16:59-65
INTRODUCTION In the heart, pathways that transduce extracellular environmental cues (e.g. mechanical force, inflammatory stress) into electrical and/or chemical signals at the cellular level are critical for the organ-level response to chronic biomec
Autor:
Drew M. Nassal, Peter J. Mohler, Jane Yu, Sathya D. Unudurthi, Thomas J. Hund, Rebecca Shaheen, Nehal J. Patel
Publikováno v:
Journal of Biological Chemistry. 297:100893
Fibrosis is a pronounced feature of heart disease and the result of dysregulated activation of resident cardiac fibroblasts (CFs). Recent work identified stress-induced degradation of the cytoskeletal protein βIV-spectrin as an important step in CF
Autor:
Drew M. Nassal, Curtis G. Pierson, Shyam S. Bansal, Evelyn Thomas, Nehal J. Patel, Peter J. Mohler, Thomas J. Hund, Jane Yu, Sathya D. Unudurthi
Publikováno v:
Life Sci
Aims Heart failure (HF) is characterized by compromised cardiac structure and function. Previous work has identified a link between upregulation of pro-inflammatory cytokines and HF. Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK)
Autor:
Benjamin W Scandling, Drew M. Nassal, Sathya D. Unudurthi, Daniel Gratz, Xianyao Xu, Federica Accornero, Thomas J. Hund, Keith J. Gooch, Peter J. Mohler, Amara Greer-Short, Anuradha Kalyanasundaram, Vadim V. Fedorov, Nehal J. Patel
Publikováno v:
JCI Insight. 4
Increased fibrosis is a characteristic remodeling response to biomechanical and neurohumoral stress and a determinant of cardiac mechanical and electrical dysfunction in disease. Stress-induced activation of cardiac fibroblasts (CFs) is a critical st
Autor:
Nehal J. Patel, Evelyn Thomas, Thomas J. Hund, Alexander J. Winkle, Sathyadev Unudurthi, Daniel Gratz
Publikováno v:
Circulation Research. 125
Heart failure (HF) is a complex disease characterized by compromised cardiac structure and function. Previous work has identified a link between upregulation of pro-inflammatory cytokines, and HF. There is a critical need to gain better understanding
Autor:
Benjamin W Scandling, Nehal J. Patel, Drew M. Nassal, Amara Greer-Short, Thomas J. Hund, Sathya D. Unudurthi, Xianyao Xu, Keith J. Gooch, Peter J. Mohler
Publikováno v:
Circulation Research. 125
Increased fibrosis is associated with cardiac dysfunction and arrhythmias. Activation of quiescent cardiac fibroblasts (CFs) occurs in response to injury although the underlying mechanistic pathways remain unclear. The cytoskeletal protein β IV -spe