The “AID Project”: Uncovering the Mysteries of Insect vasa Genes

Chun-Che Chang, a joint faculty member of NTU CDBRM, published an insightful paper in early December 2025. Through the AID (Aphid in Drosophila) Project, his group and collaborators (including Ming-Der Lin and others) uncovered novel roles of the duplicated vasa genes in aphids, which are serious agricultural pests. By expressing aphid genes in Drosophila melanogaster—one of the best-studied model organisms—the team revealed unexpected somatic functions of these duplicated aphid vasa genes, which had long been regarded as germline-specific in most insects. Chang believes that this study will shed new light on the evolutionary and developmental roles of insect germline genes. The full article is published in the Royal Entomological Society’s journal Insect Molecular Biology:https://resjournals.onlinelibrary.wiley.com/doi/10.1111/imb.70020

Prof. Nai-Chen Cheng’s group has developed the biomaterial-assisted and scaffold-free 3D culture technology for cell therapy.

Therapeutic mechanism of the ASC sheet FBS-cultured ASC sheets suppressed macrophage infiltration and exhibited an anti-scarring effect, thereby enhancing skin healing with superior quality of neo-dermis. (Yu et al. Acta Biomaterialia 2018)    Employ HPL for the ASC sheet fabrication They investigated the effect of human platelet lysate (HPL) on extracellular matrix (ECM) deposition and cellular characteristics in ASC sheets, and successfully fabricated thicker ASC sheets with enhanced ECM deposition. (Cheng et al. Front. Cell Dev. Biol. 2020) Composite ASC spheroids and sheets for engineering scaffold-free biosystems Schematic diagram of the manufacturing process of a composite ASC spheroid sheet. (Yu et al. Stem Cell Research & Therapy 2022) Investigate the biological characteristics among ASC spheroids, sheets, and 2D ASCs In the spheroid sheet construct, ASC spheroids can augment the pro-angiogenesis capability of ASC sheets without the use of exogenous biomaterial or genetic manipulation. In the spheroid sheet construct, ASC spheroids can augment the pro-angiogenesis capability of ASC sheets without the use of exogenous biomaterial or genetic manipulation. (Yu et al. Stem Cell Research & Therapy 2022) GTP-compatible ASC sheets for clinical therapeutic purposes HPL-cultured ASC sheets combined with bio-cellulose membranes are being developed as a potential treatment for diabetic ulcers. (Yu et al. Stem Cell Research & Therapy 2022)

Selective therapeutic efficacy of tyrosine kinase inhibitor sorafenib on the restoration of methylglyoxal-induced peritoneal fibrosis

Peritoneal fibrosis, a common complication observed in long-term peritoneal dialysis patients, can gradually lead to ultrafiltration failure and the development of encapsulating peritoneal sclerosis. To assess the potential therapeutic effects of tyrosine kinase inhibitors on peritoneal fibrosis in the larger animal model, a novel porcine model of peritoneal fibrosis induced by 40 mM methylglyoxal in 2.5% dialysate was established, and two different doses (20mg/kg and 30mg/kg) of sorafenib were given orally to evaluate their therapeutic efficacy in the study. We showed that sorafenib effectively reduced adhesions between peritoneal organs and significantly diminished the thickening of both the parietal and visceral peritoneum. Angiogenesis, vascular endothelial growth factor A production, myofibroblast infiltration, and decreased endothelial glycocalyx resulting from dialysate and methylglyoxal stimulations were also alleviated with sorafenib. However, therapeutic efficacy in ameliorating loss of mesothelial cells, restoring decreased ultrafiltration volume, and improving elevated small solutes transport rates was limited. In conclusion, this study demonstrated that sorafenib could potentially be used for peritoneal fibrosis treatment, but applying sorafenib alone might not be sufficient to fully rescue methylglyoxal-induced peritoneal defects.

Professor Kai-Chien Yang’s research team at the Institute of Pharmacology has discovered that N-Cadherin promotes cardiac regeneration by potentiating pro-mitotic β-Catenin signaling in cardiomyocytes

Adult human hearts exhibit limited regenerative capacity. Post-injury cardiomyocyte (CM) loss can lead to myocardial dysfunction and failure. Although neonatal mammalian hearts can regenerate, the underlying molecular mechanisms remain elusive. Herein, comparative transcriptome analyses identify adherens junction protein N-Cadherin as a crucial regulator of CM proliferation/renewal. Its expression correlates positively with mitotic genes and shows an age-dependent reduction. N-Cadherin is upregulated in the neonatal mouse heart following injury, coinciding with increased CM mitotic activities. N-Cadherin knockdown reduces, whereas overexpression increases, the proliferation activity of neonatal mouse CMs and human induced pluripotent stem cell-derived CMs. Mechanistically, N-Cadherin binds and stabilizes pro-mitotic transcription regulator β-Catenin, driving CM self-renewal. Targeted N-Cadherin deletion in CMs impedes cardiac regeneration in neonatal mice, leading to excessive scarring. N-Cadherin overexpression, by contrast, promotes regeneration in adult mouse hearts following ischemic injury. N-Cadherin targeting presents a promising avenue for promoting cardiac regeneration and restoring function in injured adult human hearts.