Related Experiment Video

Updated: Jan 22, 2026

Myocardial Infarction and Functional Outcome Assessment in Pigs
12:03

Myocardial Infarction and Functional Outcome Assessment in Pigs

Published on: April 25, 2014

28.6K

Inhibition of pro-inflammatory myeloid cell responses by short-term S100A9 blockade improves cardiac function after

Goran Marinković1, Helena Grauen Larsen2, Troels Yndigegn2

  • 1Department of Clinical Sciences Malmö, Lund University, CRC 91:12, Jan Waldenströms gata 35, SE-214 28, Malmö, Sweden.

European Heart Journal
|July 12, 2019
PubMed

Insights

Blocking S100A9 reduces inflammation and improves heart function after myocardial infarction (MI). This approach may help patients with acute coronary syndrome (ACS) and prevent heart failure (HF).

Area of Science:

  • Immunology
  • Cardiology
  • Molecular Biology

Background:

  • Neutrophils play complex roles in myocardial infarction (MI), with underlying pathways not fully understood.
  • S100A8/A9, a neutrophil-derived alarmin, is released into circulation post-myocardial ischemia, indicating its potential role in MI pathogenesis.
  • High S100A8/A9 levels in acute coronary syndrome (ACS) patients correlate with poorer cardiac function and increased heart failure (HF) risk.

Purpose of the Study:

  • To investigate the role of S100A8/A9 in the innate immune response to myocardial infarction (MI).
  • To evaluate the therapeutic potential of blocking S100A9 in preclinical models of MI.

Main Methods:

  • Analysis of plasma S100A8/A9 levels in 524 acute coronary syndrome (ACS) patients, correlating with cardiac function and heart failure (HF) hospitalization.
  • Pharmacological blockade of S100A9 using ABR-238901 in wild-type mice subjected to permanent coronary artery ligation (MI).
  • Assessment of immune cell dynamics, cardiac function (left ventricular ejection fraction, cardiac output), and inflammatory markers in treated versus untreated MI mice, including an ischemia/reperfusion model.

Main Results:

  • In ACS patients, elevated S100A8/A9 was linked to reduced left ventricular ejection fraction (EF) at 1 year and higher HF hospitalization rates.
  • S100A9 blockade in mice inhibited bone marrow stem cell proliferation and myeloid cell egress, reducing cardiac neutrophils and macrophages.
  • Treatment with ABR-238901 significantly improved cardiac function, including left ventricular EF and cardiac output, in murine MI and ischemia/reperfusion models.

Conclusions:

  • Short-term S100A9 blockade effectively reduces inflammation and enhances cardiac function in experimental models of myocardial infarction (MI).
  • The findings suggest that excessive S100A8/A9 release contributes to adverse outcomes in MI and ACS.
  • S100A9 blockade presents a promising therapeutic strategy to improve prognosis in patients with acute coronary syndrome (ACS).
Abstract

Keywords:
Inflammatory monocytesMacrophagesMyocardial infarctionNeutrophilsS100A8/A9S100A9

More Related Videos

Myocardial Infarction in Neonatal Mice, A Model of Cardiac Regeneration07:48

Myocardial Infarction in Neonatal Mice, A Model of Cardiac Regeneration

Published on: May 24, 2016

19.7K
Simultaneous 3D Analysis of Cardiac Damage and Immune Response in Reperfused Acute Myocardial Infarction Using Light Sheet Fluorescence Microscopy06:38

Simultaneous 3D Analysis of Cardiac Damage and Immune Response in Reperfused Acute Myocardial Infarction Using Light Sheet Fluorescence Microscopy

Published on: September 26, 2025

1.1K

Related Concept Videos

Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
16.1K
Inflammatory Response II: Inflammatory Exudate and Tissue Repair01:24

Inflammatory Response II: Inflammatory Exudate and Tissue Repair

The immune system's inflammatory response destroys the invading pathogen, permitting the tissue to heal. The changes during the cellular and vascular stages allow exudate formation at the site of inflammation. The inflammatory exudate released from the wound has high protein content and a specific gravity above 1.020.
The typical wound exudate is odorless, transparent, straw-colored, thin, and watery. Exudate, however, can differ depending on the state of wound healing. Likewise, the...
7.5K
Inflammatory Response I: Vascular and Cellular01:30

Inflammatory Response I: Vascular and Cellular

The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
16.2K
Neuromuscular Junction And Blockade01:29

Neuromuscular Junction And Blockade

The site of chemical communication between a motor neuron and a muscle fiber is called the neuromuscular junction (NMJ). The end of the motor neuron at the NMJ divides into a cluster of synaptic end bulbs. The cytoplasm of these bulbs consists of synaptic vesicles enclosing acetylcholine molecules, the principal neurotransmitter released at the NMJ. The region opposite the synaptic bulb that ends in the muscle fiber is called the motor end plate, which has acetylcholine receptors. Within the...
4.8K
Long-term Depression01:05

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
33.2K
Feedback Inhibition00:46

Feedback Inhibition

Biochemical reactions are occurring constantly in cells, converting starting substances to different products, usually with the help of enzymes that speed the reactions. Without enzymes, it would take far too long for most reactions to occur to be useful to the cell!
56.9K