Inflammation and fibrosis in murine models of heart failure

L Bacmeister, M Schwarzl, S Warnke, B Stoffers… - Basic research in …, 2019 - Springer
Heart failure is a consequence of various cardiovascular diseases and associated with poor
prognosis. Despite progress in the treatment of heart failure in the past decades, prevalence …

[HTML][HTML] Physiological implications of myocardial scar structure

WJ Richardson, SA Clarke, TA Quinn… - Comprehensive …, 2015 - ncbi.nlm.nih.gov
Once myocardium dies during a heart attack, it is replaced by scar tissue over the course of
several weeks. The size, location, composition, structure and mechanical properties of the …

Monocytes: protagonists of infarct inflammation and repair after myocardial infarction

M Nahrendorf, MJ Pittet, FK Swirski - Circulation, 2010 - Am Heart Assoc
Myocardial infarction (MI) is the most frequent cause of heart failure, which is an
incapacitating disease with high prevalence and broad socioeconomic impact. In 2008 in …

[HTML][HTML] Enzyme-responsive nanoparticles for targeted accumulation and prolonged retention in heart tissue after myocardial infarction

MM Nguyen, AS Carlini, MP Chien… - … (Deerfield Beach, Fla …, 2015 - ncbi.nlm.nih.gov
Herein, we describe a method for targeting to and retaining intravenously (IV) injected
nanoparticles at the site of acute myocardial infarction (MI) in a rat model. Enzyme …

Extensive scar formation and regression during heart regeneration after cryoinjury in zebrafish

JM González-Rosa, V Martín, M Peralta… - …, 2011 - journals.biologists.com
The zebrafish heart has the capacity to regenerate after ventricular resection. Although this
regeneration model has proved useful for the elucidation of certain regeneration …

Injectable human recombinant collagen matrices limit adverse remodeling and improve cardiac function after myocardial infarction

S McLaughlin, B McNeill, J Podrebarac… - Nature …, 2019 - nature.com
Despite the success of current therapies for acute myocardial infarction (MI), many patients
still develop adverse cardiac remodeling and heart failure. With the growing prevalence of …

BET bromodomain inhibition suppresses innate inflammatory and profibrotic transcriptional networks in heart failure

Q Duan, S McMahon, P Anand, H Shah… - Science translational …, 2017 - science.org
Despite current standard of care, the average 5-year mortality after an initial diagnosis of
heart failure (HF) is about 40%, reflecting an urgent need for new therapeutic approaches …

EDIL3 deficiency ameliorates adverse cardiac remodelling by neutrophil extracellular traps (NET)-mediated macrophage polarization

X Wei, S Zou, Z Xie, Z Wang, N Huang… - Cardiovascular …, 2022 - academic.oup.com
Aims After myocardial infarction (MI), injured cardiomyocytes recruit neutrophils and
monocytes/macrophages to myocardium, which in turn initiates inflammatory and reparative …

Inhibition of mitochondrial permeability transition improves functional recovery and reduces mortality following acute myocardial infarction in mice

L Gomez, H Thibault, A Gharib… - American Journal …, 2007 - journals.physiology.org
Inhibition of mitochondrial permeability transition pore (mPTP) opening by cyclosporin A or
ischemic postconditioning attenuates lethal reperfusion injury. Its impact on major post …

Near-infrared fluorescent imaging of matrix metalloproteinase activity after myocardial infarction

J Chen, CH Tung, JR Allport, S Chen, R Weissleder… - Circulation, 2005 - Am Heart Assoc
Background—We used a molecular probe activated by protease cleavage to image
expression of matrix metalloproteinases (MMPs) in the heart after myocardial infarction …