Seven trainee abstracts from the lab of Jianyi “Jay” Zhang, M.D., Ph.D., professor and T. Michael and Gillian Goodrich Endowed Chair of Engineering Leadership, were selected for the 2025 American Heart Association’s (AHA) Scientific Sessions conference.

AHA is an annual conference that showcases the latest advancements in cardiovascular science, spanning basic research, translational studies, clinical trials, and real-world applications.

Each year, thousands of scientists and clinicians from around the world participate to advance cardiovascular health, and fewer than twenty percent of submitted abstracts are accepted, making this recognition a notable achievement for the trainees and their lab.

Selected trainee abstracts

These abstracts highlight the exciting work of Zhang lab trainees, from studying heart cell biology to developing new ways to treat heart disease. Each project gives a glimpse into the innovative approaches the lab is taking to improve cardiovascular health.

Read their abstract summaries below.

Xiaoxiao Geng, Ph.D.

“Chromatin Structural Gene Expression Stratifies Cardiac Cell Populations in Health and Disease”

The structure of DNA within heart cells, called chromatin, helps control which genes are turned on and off and maintains the identity of the cells. This study looked at how genes controlling chromatin structure behave differently in healthy hearts compared with hearts affected by disease, such as dilated cardiomyopathy.

Researchers identified four distinct groups of heart cells, one of which was found only in diseased hearts. This group showed signs of disease, including weaker contraction-related genes and changes in 25 chromatin-regulating genes, including HMGN3. Further experiments confirmed that HMGN3 levels were reduced in diseased human, mouse, and pig hearts. In lab-grown human heart cells, reducing HMGN3 caused more cell death and made chromatin more compact, showing that HMGN3 helps maintain healthy cell function. These findings highlight the importance of chromatin organization in heart disease and suggest potential targets for therapy.

Bijay Guragain, Ph.D.

“High-Resolution Optical Mapping of hiPSC Cardiac Grafts in Swine Reveals Reentry and Automaticity as Potential Arrhythmia Mechanisms at the Host-Graft Interface.”

Implanting heart cells derived from human stem cells can improve heart function after a heart attack, but it is important that the new tissue integrates electrically with the patient’s heart to avoid irregular heartbeats. In this study, stem cell-derived heart tissue was implanted into pig hearts and examined one week later.

The implanted tissue conducted electrical signals about four times more slowly than the surrounding heart and had low levels of a key connecting protein, misaligned muscle fibers, and small scar areas at the interface with the host heart. While the grafted tissue could beat on its own, its signals did not consistently spread to the host heart. These findings show that newly implanted heart tissue can create conditions for potential arrhythmias, though this risk may decrease as the graft matures and integrates better with the host tissue.

Kaili Hao, Ph.D.

“Heat-shock Protein HSPA5 and HSP90B1 Were Upregulated in Pig Cardiomyocytes Responding to Apical Resection on Postnatal Day 1 and Prior to Cardiomyocyte Cell-cycle”

After a heart injury in newborn pigs, researchers found that two protective proteins, called heat-shock proteins HSPA5 and HSP90B1, become more active in heart muscle cells before these cells begin to multiply and repair the damaged tissue. These proteins help the cells respond to stress and may play a key role in triggering the heart’s natural ability to regenerate.

Using advanced gene analysis techniques, the team observed that the levels of these heat-shock proteins stayed high in injured heart cells during the early days following injury, even before cell division increased. This suggests that HSPA5 and HSP90B1 could be important in activating the molecular pathways that lead to heart muscle cell growth. The findings point to the potential for new treatments that target these proteins to improve heart repair after injury in humans.

Thanh Nguyen, Ph.D.

“RNA Binding Protein in Proliferative Cardiomyocytes: a Cross-species Meta-analysis from Mouse, Pig, and Human Transcriptomic Profiling Data”

Heart muscle cells have a limited ability to multiply after injury, but in newborn mice and pigs, these cells can regenerate following certain heart injuries. This study looked at proteins called RNA-binding proteins (RBPs), which help turn genetic instructions into functional proteins, to see if they play a role in heart cell growth.

By analyzing data from mice, pigs, and human stem cell-derived heart cells, researchers found 21 RBPs that were consistently higher in cells that were actively dividing. Further tissue studies in pigs confirmed that some of these RBPs, like DHX9 and PTBP3, were more abundant in hearts capable of regeneration. The findings suggest that RBPs are closely linked to heart cell proliferation and could be important targets for therapies aimed at repairing damaged hearts.

Yuhua Wei, Ph.D.

“Human induced pluripotent stem cell derived nanovesicles for the treatment of ischemic limb diseases”

Critical limb ischemia is a serious condition where poor blood flow can cause pain, ulcers, and increase the risk of amputation. In this study, tiny vesicles called nanovesicles, made from specially engineered human stem cells, were tested as a treatment.

The nanovesicles protected human blood vessel cells from damage and helped them grow in lab tests. When given to mice with reduced blood flow in their limbs, the treatment improved circulation, encouraged new blood vessel formation, and increased blood vessel cell growth—all without needing immune-suppressing drugs. These results suggest that stem cell-derived nanovesicles could be a promising therapy for ischemic limb disease.

Yalin Wu, Ph.D.

“TT-10–loaded Nanoparticles Promote Cardiomyocyte Proliferation and Improve Recovery from Myocardial Injury in Pig”

Adult heart muscle cells have very limited ability to repair themselves after a heart attack. A small molecule called TT-10 can stimulate these cells to re-enter the cell cycle and multiply, but it is quickly cleared from the body, limiting its effectiveness. To overcome this, TT-10 was packaged into nanoparticles that allow the drug to be delivered directly to the heart and released slowly over time.

In lab tests with human stem cell-derived heart cells, the nanoparticles activated the YAP signaling pathway, which promoted cell division. In pigs that had a heart attack, injecting TT-10 nanoparticles into the heart improved heart cell proliferation, reduced the size of the damaged area, improved heart function, and decreased heart muscle thickening compared with untreated animals. These results suggest that TT-10 nanoparticles could be a promising approach to help damaged hearts regenerate and recover after a heart attack.

Hanyu Zhang, Ph.D.

“Overexpression of Connexin-43 Improves Electrical Conduction between hiPSC-derived Cardiomyocytes”

Implanting heart muscle cells derived from human stem cells is a promising way to repair damaged hearts, but a major challenge is ensuring that the implanted cells conduct electricity in sync with the patient’s own heart. Stem cell-derived heart cells often have slower electrical signals, which can increase the risk of irregular heartbeats.

In this study, scientists boosted levels of a protein called connexin-43, which forms connections between heart cells, in stem cell-derived heart cells. The treated cells conducted electrical signals faster than untreated cells, suggesting that increasing connexin-43 could help implanted heart tissue beat in harmony with the patient’s heart. This approach may improve the safety and effectiveness of stem cell-based heart repair therapies.