Che Ping Cheng | Translational Neuroscience | Best Researcher Award

Prof. Che Ping Cheng | Translational Neuroscience | Best Researcher Award

Prof. Che Ping Cheng, Wake Forest University School of Medicine, United States.

Dr. Che Ping Cheng, M.D., Ph.D., FAHA, is a distinguished cardiovascular physiologist and internal medicine specialist whose career has been dedicated to advancing the understanding of heart function and failure. From earning his medical degree in China to completing a Ph.D. in Physiology at Wayne State University, and later conducting pivotal postdoctoral research at Wake Forest School of Medicine, Dr. Cheng has consistently pursued excellence in science and education. His research on ventricular mechanics, volume loading, and heart failure has significantly influenced both experimental cardiology and clinical practice. Recognized as a Fellow of the American Heart Association, he is also a dedicated mentor, shaping the next generation of cardiovascular researchers through his academic leadership.

Profile

Scopus

 

🎓 Early Academic Pursuits

Dr. Che Ping Cheng’s journey into medicine and science began in Nanjing, China, where he earned his M.D. degree from Nanjing Railway Medical University in 1977. His early academic path reflected a deep interest in understanding the intricacies of human health, particularly in cardiovascular physiology. Driven by a desire to expand his knowledge and research capabilities, Dr. Cheng pursued his Ph.D. in Physiology at Wayne State University School of Medicine in Detroit, Michigan, completing his degree in 1986. Under the mentorship of Dr. Robert S. Shepard, his doctoral work focused on exploring the mechanisms of cardiovascular response to volume loading in a canine model with tricuspid valvulectomy, setting a strong foundation for his lifelong focus on heart function and disease mechanisms.

🩺 Professional Endeavors

Following his academic training, Dr. Cheng embarked on postdoctoral studies at the Bowman Gray School of Medicine (now part of Wake Forest School of Medicine), where he continued to cultivate his expertise in internal medicine and cardiovascular physiology. Between 1986 and 1988, he served as a Postdoctoral Fellow under the guidance of Dr. William C. Little. His research during this period focused on ventricular dynamics and the physiological factors affecting active ventricular filling, which would later inform his broader work on heart failure and cardiac function. Dr. Cheng has since remained at Wake Forest School of Medicine, where he is currently a distinguished member of the Section on Cardiovascular Medicine.

🧪 Contributions and Research Focus

Dr. Cheng’s career has been characterized by a deep commitment to advancing the understanding of cardiac hemodynamics, ventricular interaction, and heart failure mechanisms. His research has explored how ventricular function responds under altered physiological states, and how these responses inform disease progression and treatment strategies. His early animal model studies have provided critical insights into the interplay between structural and functional changes in the heart, especially in the context of diastolic dysfunction and volume overload conditions. Dr. Cheng has also made significant strides in translating these findings to clinical contexts, influencing how cardiologists approach diagnosis and therapy.

🏅 Accolades and Recognition

Throughout his career, Dr. Cheng has received considerable recognition for his scholarly contributions. He is a Fellow of the American Heart Association (FAHA), an honor that reflects his standing in the field of cardiovascular research and his commitment to scientific excellence. His work has earned the respect of colleagues and institutions alike, leading to numerous invitations to contribute to collaborative projects, serve on peer-review panels, and mentor future generations of cardiovascular researchers.

🌍 Impact and Influence

Dr. Cheng’s work has had a lasting impact on both experimental and clinical cardiology. By elucidating the mechanistic basis of ventricular dysfunction, he has helped shift paradigms in heart failure management, particularly in the areas of ventricular interdependence and preload responsiveness. His research findings are frequently cited in textbooks and high-impact journals, and they continue to inform guidelines for cardiac care and interventions. Through his work at Wake Forest and beyond, Dr. Cheng has played a pivotal role in bridging laboratory discoveries with bedside applications.

👨‍🏫 Legacy and Mentorship

As a respected mentor and educator, Dr. Cheng has dedicated a significant portion of his career to training medical students, residents, and postdoctoral fellows. His mentorship has influenced numerous emerging scholars in cardiovascular medicine, many of whom have gone on to successful academic and clinical careers. His guidance combines a rigorous scientific approach with a deep sense of responsibility to patient care and scientific integrity, shaping a legacy that extends well beyond his own research output.

🔬 Future Contributions and Vision

Looking ahead, Dr. Cheng remains committed to the advancement of cardiovascular research, with a continued focus on uncovering the cellular and mechanical determinants of heart disease. His vision includes fostering collaborative projects that integrate biomedical engineering, imaging, and computational modeling to further understand cardiac performance. With decades of experience and a forward-thinking approach, Dr. Cheng’s future contributions are poised to leave a lasting mark on the field of translational cardiovascular medicine.

Publication

  1. Title: Increased CaMKII activation and contrast changes of cardiac β1-and β3-Adrenergic signaling pathways in a humanized angiotensinogen model of hypertension
    Authors: Sun, Xiaoqiang; Cao, Jing; Chen, Zhe; Ferrario, Carlos M.; Cheng, Cheping
    Year: 2023
    Journal: Heliyon

 

  1. Title: Calmodulin-dependent protein kinase II activation promotes kidney mesangial expansion in streptozotocin-induced diabetic mice
    Authors: Mikhailov, Alexei V.; Liu, Yixi; Cheng, Hengjie; Lin, Jen Jar; Cheng, Cheping
    Year: 2022
    Journal: Heliyon

 

  1. Title: Chronic GPR30 agonist therapy causes restoration of normal cardiac functional performance in a male mouse model of progressive heart failure: Insights into cellular mechanisms
    Authors: Zhang, Xiaowei; Li, Tiankai; Cheng, Hengjie; Groban, Leanne; Cheng, Cheping
    Year: 2021
    Journal: Life Sciences

 

  1. Title: Chronic Ca2+/calmodulin-dependent protein Kinase II inhibition rescues advanced heart failure
    Authors: Liu, Yixi; Shao, Qun; Cheng, Hengjie; Zhao, David Xiao Ming; Cheng, Cheping
    Year: 2021
    Journal: Journal of Pharmacology and Experimental Therapeutics

 

  1. Title: The Angiotensin-(1–12)/Chymase axis as an alternate component of the tissue renin angiotensin system
    Authors: Ferrario, Carlos M.; Groban, Leanne; Wang, Hao; Sun, Xuming; Ahmad, Sarfaraz
    Year: 2021
    Journal: Molecular and Cellular Endocrinology

 

  1. Title: Reversal of angiotensin-(1–12)-caused positive modulation on left ventricular contractile performance in heart failure: Assessment by pressure-volume analysis
    Authors: Li, Tiankai; Zhang, Zhi; Zhang, Xiaowei; Ferrario, Carlos M.; Cheng, Cheping
    Year: 2020
    Journal: International Journal of Cardiology

 

  1. Title: Female Heart Health: Is GPER the Missing Link?
    Authors: Groban, Leanne; Tran, Q. K.; Ferrario, Carlos M.; Wang, Hao; Lindsey, Sarah H.
    Year: (Not specified, but likely 2020 or 2021)
    Journal: (Not specified)

 

🏁 Conclusion

Dr. Cheng’s legacy is one of intellectual rigor, clinical relevance, and mentorship. His work has not only deepened the scientific understanding of cardiac physiology but has also shaped modern approaches to diagnosing and managing heart failure. With a career spanning continents and disciplines, Dr. Cheng continues to be a guiding force in cardiovascular medicine, and his future contributions are anticipated to further advance the frontiers of heart research and patient care.