Feng Jiang | Cardiovascular Pharmacology | Best Researcher Award

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Dr. Feng Jiang | Cardiovascular Pharmacology | Best Researcher Award

Stanford University | United States

Dr. Feng Jiang is a highly accomplished postdoctoral researcher at Stanford University, specializing in uncovering the mechanisms and risk factors of human autoimmune diseases. His research focuses on performing experiments and bioinformatic analyses on genetic and RNA-seq data to identify key disease mechanisms and develop therapeutics targeting these pathways. He has also established predictive models based on risk factors to enable early diagnosis of autoimmune conditions. Prior to his postdoctoral work, Dr. Jiang completed his Ph.D. at the University of Rochester, where he conducted extensive research targeting profibrotic genes to combat cardiac fibrosis. His work involved identifying common regulators controlling the expression of profibrotic genes, inhibiting their activity in animal models, and exploring the regulation of mRNA translation in cancer and heart disease. Additionally, he investigated the role of microRNAs in disease, identifying key microRNAs involved in disease progression and their potential as biomarkers for diagnosis and monitoring.Dr. Jiang also gained international research experience as a research fellow at Yat-sen University, where he executed sequencing library construction and established analysis pipelines for human and mouse samples. During his undergraduate studies at Wuhan University, he investigated the role of the gene GLIS2 in cancer progression using CRISPR/Cas9 gene editing techniques.He has contributed significantly to the scientific literature with numerous impactful publications, including works such as RNA Binding Protein PRRC2B Mediates Translation of Specific mRNAs and Regulates Cell Cycle Progression, Glutamyl-Prolyl-tRNA Synthetase Regulates Proline-Rich Pro-Fibrotic Protein Synthesis During Cardiac Fibrosis, Mammalian RNA Switches: Molecular Rheostats in Gene Regulation, Disease, and Medicine, MicroRNA574 Regulates FAM210A Expression and Influences Pathological Cardiac Remodeling, Correlation Between Severity of Spinal Stenosis and Multifidus Atrophy in Degenerative Lumbar Spinal Stenosis, Usage of Procalcitonin and sCD14-ST as Diagnostic Markers for Postoperative Spinal Infection, Correlations Between Serum P2X7, Vitamin A, 25-Hydroxy Vitamin D, and Mycoplasma Pneumoniae Pneumonia, Disruption of Tdrd5 Decouples the Stepwise Processing of Long Precursor Transcripts During Pachytene PIWI-Interacting RNA Biogenesis, and Cardiomyocyte-Specific Loss of Glutamyl-Prolyl-tRNA Synthetase Leads to Disturbed Protein Homeostasis and Dilated Cardiomyopathy.

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Featured Publications

Jiang, F., Hedaya, O. M., Khor, E. S., Wu, J., Auguste, M., & Yao, P. (n.d.). RNA binding protein PRRC2B mediates translation of specific mRNAs and regulates cell cycle progression. Nucleic Acids Research.

Wu, J., Subbaiah, K. C. V., Xie, L. H., Jiang, F., Khor, E. S., Mickelsen, D., Myers, J. R., Tang, W. H. W., & Yao, P. (n.d.). Glutamyl-prolyl-tRNA synthetase regulates proline-rich pro-fibrotic protein synthesis during cardiac fibrosis. Circulation Research.

Wu, J., Subbaiah, K. C. V., Jiang, F., Hedaya, O., Mohan, A., Yang, T., Welle, K., Ghaemmaghami, S., Tang, W. H. W., Small, E., Yan, C., & Yao, P. (n.d.). MicroRNA-574 regulates FAM210A expression and influences pathological cardiac remodeling. EMBO Molecular Medicine.

Subbaiah, K. C. V., Hedaya, O., Wu, J., Jiang, F., & Yao, P. (n.d.). Mammalian RNA switches: Molecular rheostats in gene regulation, disease, and medicine. Computational and Structural Biotechnology Journal.

Hedaya, O. M., Venkata Subbaiah, K. C., Jiang, F., Xie, L. H., Wu, J., Khor, E. S., Zhu, M., Mathews, D. H., Proschel, C., & Yao, P. (n.d.). Secondary structures that regulate mRNA translation provide insights for ASO-mediated modulation of cardiac hypertrophy. Nature Communications.

Xia, G., Li, X., Shang, Y., Fu, B., Jiang, F., Liu, H., & Qiao, Y. (n.d.). Correlation between severity of spinal stenosis and multifidus atrophy in degenerative lumbar spinal stenosis. BMC Musculoskeletal Disorders.

Zhu, X., Li, K., Zheng, J., Xia, G., Jiang, F., Liu, H., & Shi, J. (n.d.). Usage of procalcitonin and sCD14-ST as diagnostic markers for postoperative spinal infection. Journal of Orthopaedics and Traumatology.

Li, W., Li, Y., Jiang, F., & Liu, H. (n.d.). Correlation between serum levels of microRNA-21 and inflammatory factors in patients with chronic heart failure. Medicine.

Di Yang | Cardiovascular Pharmacology | Best Researcher Award

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Assoc. Prof. Dr. Di Yang | Cardiovascular Pharmacology | Best Researcher Award

Fudan University | China

Assoc. Prof. Dr. Di Yang is a distinguished researcher in the field of cardiovascular pharmacology with an academic journey beginning at Harbin Medical University, where he completed both his B.S. and M.S. degrees in Pharmacy and Pharmacology, respectively, followed by a Ph.D. in Cardiovascular Pharmacology from the School of Pharmacy, Fudan University. Currently serving as an Associate Professor at the Human Phenome Institute, Fudan University, Dr. Yang has developed a remarkable research career with postdoctoral training at Fudan University’s Basic Medical Sciences and an extensive record of competitive research grants, including multiple projects funded by the National Natural Science Foundation of China and the Shanghai Municipal Science and Technology Commission. His innovative work spans vascular biology, cardiovascular aging, epigenetics, and metabolic disorders, focusing on critical mechanisms involving pyruvate dehydrogenase kinase 4, histone methyltransferases SMYD2 and SMYD3, and m6A demethylase ALKBH5 in vascular remodeling, endothelial aging, and cardiac hypertrophy. As a prolific author, Dr. Yang has contributed significantly to high-impact journals with key publications such as The functional role of m6A demethylase ALKBH5 in cardiomyocyte hypertrophy, Poly (ADP-ribose) polymerases 16 triggers pathological cardiac hypertrophy via activating IRE1α-sXBP1-GATA4 pathway, Histone methyltransferase Smyd2 drives vascular aging by its enhancer-dependent activity, Histone methyltransferase Smyd2 drives adipogenesis via regulating STAT3 phosphorylation, H3K4 methyltransferase Smyd3 mediates vascular smooth muscle cell proliferation, migration and neointima formation, The histone methyltransferase DOT1L is a new epigenetic regulator of pulmonary fibrosis, Histone methyltransferase Smyd3 is a new regulator for vascular senescence.

Profile: Orcid

Featured Publications

Chen, M., & Yang, D. (2025). Current insights into obesity and m6A modification. Biomedicines, 13(9), 2164.

Chen, M., Su, H., Shu, M., Shen, F., Lu, Y., Wu, S., Su, Z., Yu, M., & Yang, D. (2024). The functional role of m6A demethylase ALKBH5 in cardiomyocyte hypertrophy. Cell Death & Disease, 15, 285.

Su, H., Xu, J., Su, Z., Xiao, C., Wang, J., Zhong, W., Meng, C., Yang, D., & Zhu, Y. (2023). Poly (ADP-ribose) polymerases 16 triggers pathological cardiac hypertrophy via activating IRE1α–sXBP1–GATA4 pathway. Cellular and Molecular Life Sciences, 80, 159.

Su, H., Meng, C., Xu, J., Su, Z., Xiao, C., & Yang, D. (2022). Histone methyltransferase Smyd2 drives adipogenesis via regulating STAT3 phosphorylation. Cell Death & Disease, 13, 899.