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Deletion of MAPL ameliorates septic cardiomyopathy by mitigating mitochondrial dysfunction.
J Transl Med
November 2024
Department of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Aim: Mitochondrial dysfunction is a critical factor in the pathogenesis of septic cardiomyopathy (SCM). Mitochondrial anchored protein ligase (MAPL), a small ubiquitin-like modifier (SUMO) E3 ligase, plays a significant role in mitochondrial function. However, the role of MAPL in SCM remains unclear.
View Article and Find Full Text PDFPatient mutations in DRP1 perturb synaptic maturation of cortical neurons.
bioRxiv
August 2024
Vanderbilt University, Cell and Developmental Biology, Nashville, TN.
With the advent of exome sequencing, a growing number of children are being identified with loss of function mutations in the dynamin 1 like ( gene encoding the large GTPase essential for mitochondrial fission, dynamin-related protein 1 (DRP1); these mutations result in severe neurodevelopmental phenotypes, such as developmental delay, optic atrophy, and epileptic encephalopathies. Though it is established that mitochondrial fission is an essential precursor to the rapidly changing metabolic needs of the developing cortex, it is not understood how identified mutations in different domains of DRP1 uniquely disrupt cortical development and synaptic maturation. We leveraged the power of induced pluripotent stem cells (iPSCs) harboring DRP1 mutations in either the GTPase or stalk domains to model early stages of cortical development .
View Article and Find Full Text PDFBRAF/p-ERK/p-DRP1(Ser616) Promotes Tumor Progression and Reprogramming of Glucose Metabolism in Papillary Thyroid Cancer.
Thyroid
October 2024
Department of Head and Neck Surgery, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, P.R. China.
Article Synopsis
- Papillary thyroid cancer (PTC) with the BRAF mutation leads to worse outcomes, and while BRAF inhibitors may help, drug resistance limits their effectiveness; this study explores how BRAF and DRP1 affect PTC cellular processes including growth and glucose metabolism.
- The research shows that the BRAF mutation boosts aerobic glycolysis by activating the BRAF/p-ERK/p-DRP1(Ser616) pathway, which enhances cell division and reduces cell death, contributing to the cancer’s aggressiveness.
- The study suggests that combining a glucose inhibitor (2-DG) with the BRAF inhibitor (dabrafenib) can significantly slow the progression of BRAF-positive PTC, indicating a promising new treatment strategy
De Novo Mutation in a Patient with Encephalopathy, Cardiomyopathy and Fatal Non-Epileptic Paroxysmal Refractory Vomiting.
Int J Mol Sci
July 2024
Unit of Cell Biology and Diagnosis of Mitochondrial Disorders, Laboratory of Medical Genetics, Bambino Gesù Children's Hospital IRCCS, 00146 Rome, Italy.
Mitochondrial fission and fusion are vital dynamic processes for mitochondrial quality control and for the maintenance of cellular respiration; they also play an important role in the formation and maintenance of cells with high energy demand including cardiomyocytes and neurons. The (dynamin-1 like) gene encodes for the DRP1 protein, an evolutionary conserved member of the dynamin family that is responsible for the fission of mitochondria; it is ubiquitous but highly expressed in the developing neonatal heart. De novo heterozygous pathogenic variants in the gene have been previously reported to be associated with neonatal or infantile-onset encephalopathy characterized by hypotonia, developmental delay and refractory epilepsy.
View Article and Find Full Text PDFGSDME promotes MASLD by regulating pyroptosis, Drp1 citrullination-dependent mitochondrial dynamic, and energy balance in intestine and liver.
Cell Death Differ
November 2024
The Center for Basic Research and Innovation of Medicine and Pharmacy (MOE), School of Pharmacy, Naval Medical University, Shanghai, China.
Dysregulated metabolism, cell death, and inflammation contribute to the development of metabolic dysfunction-associated steatohepatitis (MASH). Pyroptosis, a recently identified form of programmed cell death, is closely linked to inflammation. However, the precise role of pyroptosis, particularly gasdermin-E (GSDME), in MASH development remains unknown.
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