Welcome to the Wei Lab
Our research focuses on elucidating the central neuroimmune mechanisms underlying sympathetic nervous system activation and neurohumoral dysregulation in cardiovascular diseases, particularly heart failure (HF) and hypertension. We are particularly interested in the brain–heart axis and how interactions between neural circuits, immune signaling, and cellular stress responses in key cardiovascular regulatory brain regions influence autonomic and neuroendocrine function, ultimately contributing to cardiovascular dysfunction and disease progression. A major focus of our research is the hypothalamic paraventricular nucleus (PVN), a critical integrative center for sympathetic and neuroendocrine regulation. We investigate how neuroinflammatory signaling, oxidative stress, and endoplasmic reticulum (ER) stress disrupt central autonomic control, promote excessive sympathetic outflow and neurohumoral activation, and contribute to adverse cardiac remodeling and dysfunction. In particular, we seek to identify molecular pathways that govern neuroimmune interactions and neuronal regulation, with a focus on microglia-specific SHIP1 (INPP5D), a negative regulator of PI3K/Akt signaling, and mesencephalic astrocyte-derived neurotrophic factor (MANF), an ER-associated stress-response protein that modulates ER stress and its downstream inflammatory and oxidative responses. By integrating molecular and cellular biology, electrophysiological approaches, and in vivo cardiovascular and autonomic assessments, we aim to uncover fundamental mechanisms linking central neuroinflammation to sympathetic and neurohumoral dysregulation and identify novel therapeutic targets for cardiovascular diseases. An additional research direction in our laboratory is the development of innovative nanotechnology-based drug delivery systems capable of crossing the blood–brain barrier to achieve targeted delivery of therapeutic agents to cardiovascular regulatory brain regions. By overcoming the challenges of CNS drug delivery, these approaches hold promise for modulating central neuroinflammation, restoring autonomic balance, and attenuating excessive sympathetic activation, opening new avenues for brain-targeted therapies for HF and other cardiovascular diseases.
Shunguang Wei, PhD
Associate Professor
Division of Cardiovascular Medicine
Department of Internal Medicine
Featured Articles
Targeted delivery of TAPI-1 via biomimetic nanoparticles ameliorates post-infarct left ventricle function and remodeling
RORγt Mediates Angiotensin II-Induced Pressor Responses, Microglia Activation, and Neuroinflammation by Disrupting the Blood-Brain Barrier in Rats
Interleukin 17A Contributes to Blood-Brain Barrier Disruption of Hypothalamic Paraventricular Nucleus in Rats with Myocardial Infarction
IL (Interleukin)-17A Acts in the Brain to Drive Neuroinflammation, Sympathetic Activation, and Hypertension