Michigan State University researchers have engineered a miniature, beating human heart that can reproduce atrial fibrillation, opening a path to drug discovery for a condition that has seen no new treatments in three decades. The organoids, enriched with immune cells, reveal how inflammation drives arrhythmias and allow rapid testing of anti‑inflammatory therapies.

From Lab Dish to Living Heartbeat
For more than 30 years, atrial fibrillation (A‑fib) – the most common irregular heartbeat – has been treated with palliative drugs because researchers lacked a reliable human model to study the disease’s root causes. In a breakthrough published in Cell Stem Cell, a team led by Associate Professor Aitor Aguirre at Michigan State University (MSU) has created the first human heart organoid that not only beats but can be coaxed into an A‑fib rhythm.
The organoids are roughly the size of a lentil and contain chamber‑like structures, vascular networks, and even immune cells (macrophages) that mimic the heart’s natural environment. Dr. Colin O’Hern, an osteopathic medicine student, added macrophages to the organoids and triggered inflammation with cytokines, inducing irregular beats that mirror clinical A‑fib. When an anti‑inflammatory drug was introduced, the rhythm partially normalized, demonstrating the model’s therapeutic relevance.

Why This Matters
A‑fib affects an estimated 60 million people worldwide, yet no new drugs have emerged in three decades, largely because animal models fail to recapitulate human cardiac electrophysiology. The MSU organoids provide a physiologically accurate platform that:
- Reveals mechanisms – The study shows how innate immune cells contribute to arrhythmia, offering insights into the inflammatory triggers behind A‑fib.
- Accelerates drug screening – Pharmaceutical partners can now test compounds on human cardiac tissue, reducing reliance on animal studies and improving safety profiling.
- Supports precision medicine – The long‑term vision is to generate patient‑specific heart models from induced pluripotent stem cells, enabling individualized therapy design.
“Our new human heart organoid model is poised to end this 30‑year drought without any new drugs or therapies,” Aguirre said.
From Bench to Bedside
The organoids have already attracted collaborations with biotech and pharma companies focused on cardiotoxicity screening and arrhythmia therapeutics. By exposing the organoids to pro‑inflammatory stimuli that drive A‑fib, researchers can now evaluate whether candidate drugs mitigate or exacerbate the condition before clinical trials.
The research aligns with the National Institutes of Health’s New Approach Methodologies initiative, which seeks to modernize translational science by replacing animal models with human‑based systems.

A Glimpse of the Future
Beyond A‑fib, the technology could illuminate the origins of congenital heart defects and other rhythm disorders. The Aguirre lab is already exploring “assembloids” – composite organoids that integrate heart muscle cells with immune cells – and envisions transplant‑ready heart tissue in the long term.
The breakthrough underscores how interdisciplinary collaboration—stem cell biology, immunology, and bioengineering—can transform a stubborn clinical challenge into a tractable laboratory problem.

Source: Michigan State University, Cell Stem Cell (2025).

Comments
Please log in or register to join the discussion