Dr. Di Wen, a dedicated neurologist at the Second Hospital of Hebei Medical University, specializes in neurodegenerative diseases, particularly amyotrophic lateral sclerosis (ALS). Her research focuses on gene therapy, autophagy, and mitochondrial protection, with significant findings on the role of OPTN in regulating autophagy and mitophagy. She has contributed to multiple high-impact SCI-indexed publications and leads projects funded by the Hebei Natural Science Foundation. As a member of professional medical committees, Dr. Wen’s work advances therapeutic strategies for ALS, aiming to translate laboratory discoveries into effective clinical interventions that improve patient outcomes.

Author Profile

Scopus

Education

Dr. Di Wen’s journey into the world of neuroscience began with a strong academic foundation rooted in medical sciences, leading to her specialization in neurology. From the early stages of her education, she displayed a keen interest in understanding the complexities of the human nervous system, with a particular focus on neurodegenerative disorders. Her academic path was characterized by rigorous training, in-depth research engagements, and a determination to explore the molecular and cellular underpinnings of diseases like amyotrophic lateral sclerosis (ALS). During her early career, she cultivated expertise in advanced research methodologies, live-cell imaging techniques, and genetic intervention strategies, all of which laid the groundwork for her future breakthroughs in gene therapy and mitochondrial biology.

Experience

As a neurologist at the Department of Neurology, The Second Hospital of Hebei Medical University, Dr. Wen has combined clinical practice with high-level research. Her role bridges patient care and scientific discovery, ensuring that her laboratory findings are guided by real-world medical needs. Beyond her clinical duties, she actively engages in research projects funded by the Hebei Natural Science Foundation (Project Code: H2021206048), where she leads investigations into the genetic and molecular mechanisms underlying ALS. Dr. Wen also collaborates extensively with multidisciplinary teams, including molecular biologists, geneticists, and pharmacologists, to accelerate the translation of benchside discoveries into bedside therapies. Her professional trajectory demonstrates a rare balance of medical excellence and scientific innovation.

Research Focus

Dr. Wen’s research is centered on neurodegenerative diseases, with a primary emphasis on ALS, a condition marked by progressive motor neuron degeneration leading to paralysis. Her landmark studies have shed light on the role of the OPTN gene in regulating autophagy and mitophagy—two crucial cellular processes involved in maintaining neuronal health. Using advanced genetic tools such as LV-sgRNA-OPTN and confocal live-cell imaging, she demonstrated how loss of OPTN impairs mitochondrial function, decreases autophagic flux, and increases oxidative stress in neuronal cells. Her work extends beyond cellular models, exploring gene therapy interventions in SOD1-G93A transgenic mice, where she has shown that enhancing autophagy pathways can protect mitochondria and potentially slow ALS progression. In parallel, Dr. Wen has contributed to research on insulin-like growth factor 1 (IGF-1) as a neuroprotective agent, identifying its role in mitochondrial preservation and apoptosis inhibition. Her prolific publication record in high-impact journals like The FEBS Journal and Brain Research Bulletin underscores the depth and significance of her contributions to the global ALS research community.

Awards and Recognition

Dr. Wen’s dedication to advancing neurological research has been recognized through multiple scientific publications indexed in SCI and other reputable databases. Her papers, some of which have achieved high citation counts, reflect both her innovative approach and her influence in the field of neurobiology. She holds professional memberships in the Sleep and Mood Disorders Professional Committee of Hebei Geriatric Association and the Young Physicians Committee of Hebei Medical Association, affirming her active engagement in professional and academic communities. These affiliations enable her to contribute to collaborative research networks and participate in shaping clinical and research agendas at regional and national levels.

Impact and Influence

The impact of Dr. Wen’s work extends beyond the laboratory, influencing both clinical strategies and future research directions for ALS and related neurodegenerative disorders. By elucidating the molecular mechanisms behind impaired autophagy and mitochondrial dysfunction, she has opened new therapeutic avenues for slowing disease progression. Her studies on gene therapy interventions have the potential to revolutionize treatment protocols, offering hope to patients and their families. Furthermore, her research fosters cross-disciplinary collaboration, encouraging the integration of neurology, genetics, and molecular biology in tackling complex neurological conditions.

Publications

OPTN gene therapy increases autophagy and protects mitochondria in SOD1‐G93A‐expressing transgenic mice and cells.

Author:Wen D; Ji Y; Yuanyuan Li; Duan W; Wang Y; Li Z; Tao M; Li Y
Journal: The FEBS Journal
Year:  2024

The role of insulin-like growth factor 1 in ALS cell and mouse models: A mitochondrial protector.

Author: Wen D; Cui C; Duan W; Wang W; Wang Y; Liu Y; Li Z; Li C
Journal: Brain Research Bulletin
Year: 2019

Systemic administration of scAAV9-IGF1 extends survival in SOD1G93A ALS mice via inhibiting p38 MAPK and the JNK-mediated apoptosis pathway.

Author: Wang W; Wen D; Duan W; Yin J ; Cui C; Wang Y; Liu Y; Li C
Journal: Brain Research Bulletin
Year: 2017

TBK1 is involved in M-CSF-induced macrophage polarization through mediating the IRF5/IRF4 axis.

Author: Li Y, Ji L, Liu C, Li J, Wen D, Li Z , Yu L, Guo M, Zhang S, Duan W , Yi L, Y. Bi Y, Bu H, Li C and Liu Y
Journal:The FEBS Journal
Year: 2024

Intrathecal Delivery of ssAAV9-DAO Extends Survival in SOD1G93A ALS Mice.

Author: Wang W, Duan W, Wang Y, Wen D, Liu Y, Li Z, Hu H, Cui H, Cui C, Lin H, Li C
Journal: Neurochem Research
Year: 2017