#cardiomyocytes

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Heart-saving Movement

Mitochondrial enzymes move into the heart muscle cell nucleus as a protective response against chemotherapy-induced heart damage – potential target to alleviate heart damage in cancer patients

Read the published research paper here

Image adapted by a third party from work by Shubhi Srivastava and colleagues

Department of Biochemistry and Molecular Genetics, The University of Illinois College of Medicine, Chicago, IL, USA

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Nature Communications, July 2023

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Research reveals new insights into why the heart does not repair itself

Heart muscle is one of the least renewable tissues in the body, which is one of the reasons that heart disease is the leading cause of death for both men and women in the United States, according to the Centers for Disease Control and Prevention. Inspired by the idea of helping the heart repair itself, researchers at Baylor College of Medicine and the Texas Heart Institute have studied pathways known to be involved in heart cell functions and discovered a previously unknown connection between processes that keep the heart from repairing itself. This finding, published in the journal Nature, opens the possibility of developing strategies that will promote heart cell renewal in the future.

"We are investigating the question of why the heart muscle doesn't renew," said senior author Dr. James Martin, professor and Vivian L. Smith Chair in Regenerative Medicine at Baylor College of Medicine. "In this study, we focused on two pathways of cardiomyocytes or heart cells; the Hippo pathway, which is involved in stopping renewal of adult cardiomyocytes, and the dystrophin glycoprotein complex (DGC) pathway, essential for cardiomyocyte normal functions.

More information: Yuka Morikawa et al, Dystrophin glycoprotein complex sequesters Yap to inhibit cardiomyocyte proliferation, Nature (2017).  DOI: 10.1038/nature22979

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Growing Heart

Growing up in a supportive environment is at the heart of healthy, happy development. This is true for our hearts as well, and scientists engineering heart tissue from stem cells (starter cells with limitless development potential) for use in research and healthcare are trying to create that perfect environment. Engineered heart tissue is often limited because the cells don’t fully mature, restricting their use. A new 3D printing technique using an electric field to precisely deposit materials and create complex structures has produced an ideal microenvironment to support maturation, like a loving home or enriching school. Heart tissue grew along the structure (pictured, with fibrous actin in red and a heart cell protein in green) and showed mature cell behaviours. Scaffolds like this could help create new tissue to repair damage rather than relying on scarce donor hearts, and also provide material for tests of new potential treatments.

Written by Anthony Lewis

Image from work by Guangming Zhang and colleagues

Shandong Engineering Research Center for Additive Manufacturing, Qingdao University of Technology, Qingdao, China

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Advanced Science, February 2023

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Replacement Pump

If a zebrafish’s heart gets damaged, there’s a good chance the cells will fully regenerate, just as those pictured have done. Unfortunately, the same isn’t true for humans and, if a person survives a heart attack, they are stuck with a suboptimal pump for the remainder of their lives. Because a damaged human heart can ultimately weaken and fail, scientists are investigating cell replacement therapies to restore muscle function. One problem is, lab-grown heart cells don’t fully mature and so fail to work within the existing muscle. Recently, scientists have discovered the machinery in regenerating zebrafish heart cells necessary for their maturation, integration and function. When the equivalent machinery was switched on in lab-grown human and mouse heart cells, they showed similar signs of maturity. The next step, then, is to see whether this maturation machinery can promote the cells’ functional integration the way it does in the fish.

Written by Ruth Williams

Image from work by Phong D. Nguyen and colleagues

Hubrecht Institute-KNAW and University Medical Center Utrecht, Utrecht, Netherlands

Image copyright held by the original authors

Research published in Science, May 2023

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Bleeding Edge

During a heart attack, oxygen can't reach an area of heart tissue, and the cells there die. The long-term health of survivors depends on the border zone between injured low-oxygen cells and healthy high-oxygen ones. After a heart attack, this region goes through changes that can stop the heart from pumping blood around the body properly. But scientists haven't been able to study the border zone in detail – until now. Here, we see rat heart cells on a chip, aligned so that they can contract like a real beating heart. To mimic the border zone after a heart attack, scientists control oxygen levels in a gradient across the chip. This technology captures the damage seen in real life, including inflammation, weak contractions, and disrupted calcium signalling. Using this chip, researchers hope to understand how an oxygen gradient leads to heart failure and discover new treatments to prevent it.

Written by Henry Stennett

Image from work by Megan L. Rexius-Hall and colleagues

Laboratory for Living Systems Engineering, Department of Biomedical Engineering, USC Viterbi School of Engineering, University of Southern California, Los Angeles, CA, USA

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Science Advances, December 2022

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To the Beat

Swimming like a fish, this biohybrid device, blending artificial and biological structures, is the latest tool designed by scientists studying the heart. Powering a fish shape made of paper and gelatine, with plastic fins, are two layers of cardiac muscle cells, derived from human stem cells. When cells in one layer contract, the others stretch, activating mechanosensitive ion channels in their cell membranes that cause them to contract in return, stretching the other side, and so on, in a continuous loop propelling the fish forward of its own accord. Researchers also engineered a group of cells to drive the rhythm of contractions, acting like the sinoatrial node, the heart’s natural pacemaker. Emulating the heart’s coordinated, autonomous beating, the fish remained active for over 100 days, and even improved its performance, swimming faster over its first month of activity. Monitoring its behaviour presents new opportunities to test how cardiac muscle operates.

Written by Emmanuelle Briolat

Video by Keel Yong Lee, Sung-Jin Park, David G. Matthews, George Lauder and Kevin Kit Parker

Disease Biophysics Group, John A. Paulson School of Engineering and Applied Sciences, Harvard University, Boston, MA, USA

Video originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Research published in Science, February 2022

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Colourful Heart

If you raise your arm in the air, could the heart on your sleeve fall onto the chip on your shoulder? Heart-on-a-chip is actually a small construction that reproduces key mechanisms of the heart in order to test medicines quickly, and better understand the behaviour of heart cells. Simplifying the system while improving the accuracy of imitation and ease of use would widen the accessibility of the technology, broadening use and accelerating treatment development. A new approach employs a structural colour hydrogel – a material that changes colour depending on shape – on the reverse of a sheet of aligned nanotubes, on which heart cells grow. The shape and conductive properties of the sheet allow heart cells to align neatly and beat in time with each other, with a brilliant colour change accompanying each sheet-folding beat (pictured). It’s a living, beating, visual testing platform for a wide range of diseases and treatments.

Written by Anthony Lewis

Video from work by Lingyu Sun and colleagues

Department of Rheumatology and Immunology, Institute of Translational Medicine, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China

Video originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Advanced Science, March 2022

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A Thick Heart

With abnormally thick muscle, hearts of patients with the genetic disease hypertrophic cardiomyopathy (HCM) work harder to pump blood around the body, which can cause a variety of symptoms, and even sudden death. As part of an investigation into how HCM genetic mutations affect the heart, a cardiac magnetic resonance imaging (CMR) scan was carried out on 40,000 UK Biobank participants. This scan produces detailed images of the structures of the heart. Artificial intelligence (AI), in combination with CMR imaging, was then used to measure the thickness of the heart muscle – the rings seen here tracking the heart’s contours. Combining the imaging results with patient genetic information has enabled researchers to identify those people more likely to experience an adverse cardiac event in the future. Where patients possessed specific HCM genetic mutations, the researchers found their heart muscle was thicker and that these physical changes occurred before symptoms were experienced.

Written by Daniella Gimbosh

Video by Declan O’Regan, MRC LMS, and Dr Wenjia Bai, Imperial College Department of Brain Sciences

MRC London Institute of Medical Sciences, Imperial College London, London, UK

Video copyright held by the original authors

Research published in the Journal of the American College of Cardiology, September 2021

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