Shuai Ye
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Shuai Ye has a total of 24 co-authors. Here are the top co-authors by number of shared publications:
Bing Li
Research Center for Clinical Medicine, Jinshan Hospital Affiliated to Fudan University, Shanghai, China
1 shared publicationChang Li
Shanghai Pudong Hospital & Department of Pharmaceutics, School of Pharmacy, Key Laboratory of Smart Drug Delivery, Ministry of Education, State Key Laboratory of Advanced Drug Formulations for Overcoming Delivery Barriers, Fudan University, Shanghai, China
1 shared publicationChen Huang
Basic Medicine Experimental Teaching Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China
1 shared publicationChuchu Ma
Shanghai Pudong Hospital & Department of Pharmaceutics, School of Pharmacy, Key Laboratory of Smart Drug Delivery, Ministry of Education, State Key Laboratory of Advanced Drug Formulations for Overcoming Delivery Barriers, Fudan University, Shanghai, China
1 shared publicationFenfen Ma
Shanghai Pudong Hospital & Department of Pharmaceutics, School of Pharmacy, Key Laboratory of Smart Drug Delivery, Ministry of Education, State Key Laboratory of Advanced Drug Formulations for Overcoming Delivery Barriers, Fudan University, Shanghai, China
1 shared publicationFeng Zeng
Department of Neurosurgery, Changzheng Hospital, Naval Medical University, Shanghai, China
1 shared publication
Latest Publications
- Open Access
- 4 May 2026
- Published by Springer Nature in Nature Communications
- Vol. 17 (1)
Self-assembling scaffolds epigenetically reactivate and electroactively guide neuronal regeneration to restore central neural circuits
Central nervous system (CNS) injury is a leading cause of death and long-term disability worldwide. Neurological deficits reflect disruption of central neural circuits. A major barrier to circuit repair is the intrinsically low regenerative potential of adult CNS neurons—linked in part to failure of injury-induced nuclear export of class IIa histone deacetylases (notably HDAC5)—together with a hostile post-injury microenvironment. Here we present a multifunctional nanosystem, encapsulating the class IIa HDAC4/5-selective inhibitor LMK-235 and featuring an electroactive polyaniline coating with asymmetrically distributed 5-hydroxytryptamine moieties. Upon reaching the lesion, our nanosystem assembles into large-pore scaffolds that (i) inhibit the activity of nuclear-retained class IIa HDACs in neurons and thereby reactivate intrinsic regenerative programs, (ii) regulate microglial activation to mitigate neuroinflammation, and (iii) provide an electroactive interface promoting activity-dependent synaptic reconnection. This multi-pronged approach illustrates an integrated platform with translational potential for CNS disorders in which circuit disconnection constrains recovery.
- 4 May 2026
- Published by Springer Nature in Nature Communications
- Vol. 17 (1)
Open AccessSelf-assembling scaffolds epigenetically reactivate and electroactively guide neuronal regeneration to restore central neural circuits
Central nervous system (CNS) injury is a leading cause of death and long-term disability worldwide. Neurological deficits reflect disruption of central neural circuits. A major barrier to circuit repair is the intrinsically low regenerative potential of adult CNS neurons—linked in part to failure of injury-induced nuclear export of class IIa histone deacetylases (notably HDAC5)—together with a hostile post-injury microenvironment. Here we present a multifunctional nanosystem, encapsulating the class IIa HDAC4/5-selective inhibitor LMK-235 and featuring an electroactive polyaniline coating with asymmetrically distributed 5-hydroxytryptamine moieties. Upon reaching the lesion, our nanosystem assembles into large-pore scaffolds that (i) inhibit the activity of nuclear-retained class IIa HDACs in neurons and thereby reactivate intrinsic regenerative programs, (ii) regulate microglial activation to mitigate neuroinflammation, and (iii) provide an electroactive interface promoting activity-dependent synaptic reconnection. This multi-pronged approach illustrates an integrated platform with translational potential for CNS disorders in which circuit disconnection constrains recovery.