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GDF11 improves cardiac repair after myocardial infarction by reducing Macrophage infiltration and attenuating their inflammatory Properties.
Int Immunopharmacol
January 2025
Department of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China; State Key Laboratory of Transvascular Implantation Devices, China; Heart Regeneration and Repair Key Laboratory of Zhejiang province, China; Binjiang Institute of Zhejiang University, Hangzhou 310053, China. Electronic address:
An RNA editing strategy rescues gene duplication in a mouse model of MECP2 duplication syndrome and nonhuman primates.
Nat Neurosci
January 2025
HuidaGene Therapeutics Inc., Shanghai, China.
Duplication of methyl-CpG-binding protein 2 (MECP2) gene causes MECP2 duplication syndrome (MDS). To normalize the duplicated MECP2 in MDS, we developed a high-fidelity Cas13Y (hfCas13Y) system capable of targeting the MECP2 (hfCas13Y-gMECP2) messenger RNA for degradation and reducing protein levels in the brain of humanized MECP2 transgenic mice. Moreover, the intracerebroventricular adeno-associated virus (AAV) delivery of hfCas13Y-gMECP2 in newborn or adult MDS mice restored dysregulated gene expression and improved behavior deficits.
View Article and Find Full Text PDFGrowth differentiation factor 11 alleviates oxidative stress-induced senescence of endothelial progenitor cells via activating autophagy.
Stem Cell Res Ther
October 2024
Department of Anatomy, Histology and Embryology, Shanghai Medical School of Fudan University, 138 Yixueyuan Road, Shanghai, 200032, People's Republic of China.
Article Synopsis
- Stem cell transplantation shows potential for heart regeneration after a heart attack, but success is limited due to the harsh conditions stem cells face in the damaged heart tissue; recent research is looking at ways to improve stem cell survival and function.* -
- The study investigated the effects of GDF11 on reducing oxidative stress-related aging in endothelial progenitor cells (EPCs) that were exposed to oxidative stress, aiming to understand how to better support these stem cells post-transplantation.* -
- Results indicated that GDF11 treatment reduced oxidative damage and senescence in EPCs, improved autophagy, and enhanced heart regeneration and blood vessel formation when EPCs were transplanted into heart tissue, suggesting a promising role for GDF11 in
Growth Differentiation Factor 11 Evokes Lung Injury, Inflammation, and Fibrosis in Mice through the Activin A Receptor Type II-Like Kinase, 53kDa-Smad2/3 Signaling Pathway.
Am J Pathol
November 2024
Department of Rheumatology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. Electronic address:
Growth differentiation factor 11 (GDF11) belongs to the transforming growth factor beta superfamily and participates in various pathophysiological processes. Initially, GDF11 was suggested to act as a rejuvenator by improving age-related phenotypes of the heart, brain, and skeletal muscle in aged mice. Recent studies demonstrate that GDF11 also serves as an adverse risk factor for human frailty and diseases.
View Article and Find Full Text PDFGDF11 improves hippocampal neurogenesis and cognitive abilities in diabetic mice by reducing neural inflammation.
Brain Behav Immun
August 2024
Shenzhen United Imaging Research Institute of Innovative Medical Equipment, Shenzhen 518048, PR China. Electronic address:
Background: The cognitive decline associated with type 2 diabetes (T2D) is often attributed to compromised hippocampal neurogenesis and exacerbated neural inflammation. This study investigates the therapeutic potential of growth differentiation factor 11 (GDF11) in reversing these neurodegenerative processes in diabetic mice.
Result: We utilized a murine model of T2D and examined the effects of GDF11 on learning, memory, neurogenesis, and neuroinflammatory markers.
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