Inflamed heart with disrupted electrical activity

Inflammation's Hidden Heart Risk: How IL-6 Impacts Your Cardiac Health

"Discover the newly uncovered link between inflammation, Interleukin-6 (IL-6), and acquired Long QT Syndrome (LQTS), revealing potential risks for cardiac arrhythmias and sudden cardiac death."


Inflammation isn't just about swelling and pain; it can significantly impact your heart. Interleukin-6 (IL-6), a protein that drives inflammation, has been linked to a higher risk of acquired Long QT Syndrome (LQTS). LQTS is a condition that messes with your heart's electrical system, potentially leading to life-threatening arrhythmias. Understanding this connection is crucial for those with chronic inflammatory conditions.

If you're dealing with an autoimmune disorder like rheumatoid arthritis or another chronic inflammatory condition, your body's IL-6 levels might be elevated. Studies have shown that these elevated levels can interfere with the heart's normal rhythm, making you more vulnerable to dangerous heart rhythms like Torsades de Pointes (TdP). This type of arrhythmia can lead to sudden cardiac death, so recognizing the risk is essential.

Recent research has pinpointed exactly how IL-6 throws off your heart's rhythm. It turns out that IL-6 can suppress a critical heart channel known as hERG, which regulates the flow of potassium and is essential for proper cardiac repolarization. When hERG doesn't function correctly, it prolongs the heart's QT interval, setting the stage for arrhythmias. This breakthrough offers new targets for therapies aimed at preventing these dangerous outcomes.

The IL-6 and hERG Connection: What the Science Says

Inflamed heart with disrupted electrical activity

The study published in PLOS ONE by Aromolaran et al. (2018) provides a detailed look at the connection between IL-6 and cardiac risks. Researchers found that IL-6 directly affects the hERG channel, which is encoded by the KCNH2 gene. This channel is responsible for the rapid component of the delayed rectifier potassium current (Ikr), which helps your heart cells recharge electrically after each beat.

Using both HEK293 cells (a type of human cell commonly used in research) and heart cells from guinea pigs, scientists discovered that IL-6 reduces the function of the hERG channel. This reduction in hERG activity can prolong the action potential duration (APD), which is the time it takes for your heart cells to electrically activate and then recover. A prolonged APD contributes directly to QT prolongation and increases the risk of arrhythmias.

  • IL-6 Inhibits hERG: IL-6, especially when combined with its soluble receptor IL-6R, significantly reduces the density of Ikr, both peak and tail currents, in HEK293 cells.
  • Pathway Discovered: The team found that the disruptive effects of IL-6 could be reversed by blocking IL-6R or inhibiting Janus kinase (JAK), a key player in the IL-6 signaling pathway.
  • Real Heart Cells Affected: In guinea pig heart cells, IL-6 not only prolonged APD but also reduced the amount of ERG channel mRNA and protein, further impairing heart function.
The researchers also explored the molecular mechanisms behind this phenomenon. They found that IL-6 activates the IL-6R and JAK pathway, which then reduces hERG channel expression and function. By blocking this pathway, scientists could prevent IL-6 from disrupting the heart's electrical activity, opening doors for new treatments aimed at maintaining a healthy heart rhythm in people with inflammatory conditions.

What This Means for You

For individuals with chronic inflammatory diseases, understanding the link between IL-6 and heart rhythm disturbances is crucial. If you have conditions like rheumatoid arthritis, lupus, or other autoimmune disorders, managing your inflammation is not just about easing joint pain or other symptoms; it's also about protecting your heart. Regular check-ups, including ECGs, can help monitor your heart's electrical activity. By working closely with your healthcare provider, you can take proactive steps to minimize your risk and maintain optimal heart health.

About this Article -

This article was crafted using a human-AI hybrid and collaborative approach. AI assisted our team with initial drafting, research insights, identifying key questions, and image generation. Our human editors guided topic selection, defined the angle, structured the content, ensured factual accuracy and relevance, refined the tone, and conducted thorough editing to deliver helpful, high-quality information.See our About page for more information.

This article is based on research published under:

DOI-LINK: 10.1371/journal.pone.0208321, Alternate LINK

Title: Interleukin-6 Inhibition Of Herg Underlies Risk For Acquired Long Qt In Cardiac And Systemic Inflammation

Subject: Multidisciplinary

Journal: PLOS ONE

Publisher: Public Library of Science (PLoS)

Authors: Ademuyiwa S. Aromolaran, Ujala Srivastava, Alessandra Alí, Mohamed Chahine, Deana Lazaro, Nabil El-Sherif, Pier Leopoldo Capecchi, Franco Laghi-Pasini, Pietro Enea Lazzerini, Mohamed Boutjdir

Published: 2018-12-06

Everything You Need To Know

1

What is Interleukin-6 (IL-6), and why is it important to understand its role in heart health?

Interleukin-6 (IL-6) is a protein in the body that drives inflammation. It's important because elevated levels of IL-6 have been linked to an increased risk of acquired Long QT Syndrome (LQTS). This connection is significant because it highlights how inflammation can directly impact heart health, potentially leading to dangerous arrhythmias and sudden cardiac death. The implication is that managing inflammation is crucial for individuals with chronic inflammatory conditions to protect their heart health.

2

What is Long QT Syndrome (LQTS), and why should people be concerned about it?

Long QT Syndrome (LQTS) is a condition that affects the heart's electrical system. It is significant because it can lead to life-threatening arrhythmias, such as Torsades de Pointes (TdP), which can cause sudden cardiac death. The relevance of LQTS in the context of inflammation is that elevated levels of Interleukin-6 (IL-6), often seen in chronic inflammatory conditions, can increase the risk of developing acquired LQTS. If left unmanaged, this can substantially elevate the risk of cardiac events.

3

What is the hERG channel, and why is it important for heart function?

The hERG channel is a critical component of heart cells that regulates the flow of potassium, which is essential for proper cardiac repolarization. It is significant because its proper function ensures that the heart's electrical activity is stable and rhythmic. Interleukin-6 (IL-6) can suppress hERG, leading to prolonged action potential duration (APD), QT prolongation and increasing the risk of arrhythmias. Therefore, hERG is crucial for maintaining a healthy heart rhythm, particularly in the presence of inflammation.

4

What is the JAK pathway, and how does it relate to the effects of IL-6 on the heart?

The JAK pathway, or Janus kinase pathway, is a key signaling pathway activated by Interleukin-6 (IL-6). When IL-6 binds to its receptor (IL-6R), it activates JAK, which then reduces hERG channel expression and function. By blocking this pathway, scientists can prevent IL-6 from disrupting the heart's electrical activity. The implications are that targeting the JAK pathway could lead to new treatments aimed at maintaining a healthy heart rhythm in people with inflammatory conditions.

5

Who is most at risk from the effects of IL-6 on heart rhythm, and what can they do to protect themselves?

Individuals with chronic inflammatory conditions, such as rheumatoid arthritis, lupus, or other autoimmune disorders, are more vulnerable to heart rhythm disturbances due to elevated levels of Interleukin-6 (IL-6). Managing inflammation is critical for these individuals because high IL-6 levels can interfere with the heart's normal rhythm and increase the risk of acquired Long QT Syndrome (LQTS) and dangerous arrhythmias. Regular check-ups, including ECGs, can help monitor heart health and allow for proactive steps to minimize risk.

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