Mareike Staudt

Aachen, NW, Germany

Last Updated: 09/26/2026

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Found 14 publications

Cardiac Repair after Myocardial Infarction is Controlled by a Complement C5a Receptor 1-Driven Signaling Cascade.

Cardiac Repair after Myocardial Infarction is Controlled by a Complement C5a Receptor 1-Driven Signaling Cascade.

Journal: Thrombosis and haemostasis
Published: October 04, 2024

Endogenous Modulation of Extracellular Matrix Collagen during Scar Formation after Myocardial Infarction.

Endogenous Modulation of Extracellular Matrix Collagen during Scar Formation after Myocardial Infarction.

Journal: International journal of molecular sciences
Published: September 29, 2022

Phosphatidylserine Supplementation as a Novel Strategy for Reducing Myocardial Infarct Size and Preventing Adverse Left Ventricular Remodeling.

Phosphatidylserine Supplementation as a Novel Strategy for Reducing Myocardial Infarct Size and Preventing Adverse Left Ventricular Remodeling.

Journal: International journal of molecular sciences
Published: March 30, 2021

Induction of Accelerated Atherosclerosis in Mice: The "Wire-Injury" Model.

Induction of Accelerated Atherosclerosis in Mice: The "Wire-Injury" Model.

Journal: Journal of visualized experiments : JoVE
Published: September 14, 2020

Neutrophils Modulate Fibroblast Function and Promote Healing and Scar Formation after Murine Myocardial Infarction.

Neutrophils Modulate Fibroblast Function and Promote Healing and Scar Formation after Murine Myocardial Infarction.

Journal: International journal of molecular sciences
Published: April 16, 2020

Cardiac FGF23: new insights into the role and function of FGF23 after acute myocardial infarction.

Cardiac FGF23: new insights into the role and function of FGF23 after acute myocardial infarction.

Journal: Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
Published: October 11, 2018

Blocking CCL5-CXCL4 heteromerization preserves heart function after myocardial infarction by attenuating leukocyte recruitment and NETosis.

Blocking CCL5-CXCL4 heteromerization preserves heart function after myocardial infarction by attenuating leukocyte recruitment and NETosis.

Journal: Scientific reports
Published: November 21, 2017

Hemocompatibility of plasma electrolytic oxidation (PEO) coated Mg-RE and Mg-Zn-Ca alloys for vascular scaffold applications.

Hemocompatibility of plasma electrolytic oxidation (PEO) coated Mg-RE and Mg-Zn-Ca alloys for vascular scaffold applications.

Journal: Materials science & engineering. C, Materials for biological applications
Published: November 09, 2017

Differences in peripheral myelin antigen-specific T cell responses and T memory subsets in atypical versus typical CIDP.

Differences in peripheral myelin antigen-specific T cell responses and T memory subsets in atypical versus typical CIDP.

Journal: BMC neurology
Published: November 09, 2016

Nano-level morphology of scar tissue after myocardial infarction.

Nano-level morphology of scar tissue after myocardial infarction.

Journal: Discoveries (Craiova, Romania)
Published: September 30, 2015

Blockade of CCR3 retains the neutrophils, preserving their survival during healing after myocardial infarction.

Blockade of CCR3 retains the neutrophils, preserving their survival during healing after myocardial infarction.

Journal: Discoveries (Craiova, Romania)
Published: June 30, 2015

Minimal invasive surgical procedure of inducing myocardial infarction in mice.

Minimal invasive surgical procedure of inducing myocardial infarction in mice.

Journal: Journal of visualized experiments : JoVE
Published: May 21, 2015
Showing 1-12 of 14

Last Updated: 09/26/2026