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Mitochondrial apoptosis in response to cardiac ischemia-reperfusion injury.
J Transl Med
January 2025
Department of Cardiovascular Ultrasound, The First Hospital of China Medical University, Shenyang, China.
In patients with acute myocardial infarction (AMI), thrombolytic therapy and revascularization strategies allow complete recanalization of occluded epicardial coronary arteries. However, approximately 35% of patients still experience myocardial ischemia/reperfusion (I/R) injury, which contributing to increased AMI mortality. Therefore, an accurate understanding of myocardial I/R injury is important for preventing and treating AMI.
View Article and Find Full Text PDFPrP Glycoprotein Is Indispensable for Maintenance of Skeletal Muscle Homeostasis During Aging.
J Cachexia Sarcopenia Muscle
February 2025
Department of Bioactive Material Sciences, Research Center of Bioactive Materials, Jeonbuk National University, Jeonju, Republic of Korea.
Background: The cellular prion protein (PrP), a glycoprotein encoded by the PRNP gene, is known to modulate muscle mass and exercise capacity. However, the role of PrP in the maintenance and regeneration of skeletal muscle during ageing remains unclear.
Methods: This study investigated the change in PrP expression during muscle formation using C2C12 cells and evaluated muscle function in Prnp wild-type (WT) and knock-out (KO) mice at different ages (1, 9 and 15 months).
Aptamer-Conjugated Exosomes Ameliorate Diabetes-Induced Muscle Atrophy by Enhancing SIRT1/FoxO1/3a-Mediated Mitochondrial Function.
J Cachexia Sarcopenia Muscle
February 2025
Department of Endocrinology and Metabolism, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Background: Muscle atrophy is associated with Type 2 diabetes mellitus, which reduces the quality of life and lacks effective treatment strategies. Previously, it was determined that human umbilical cord mesenchymal stromal cell (hucMSC)-derived exosomes (EXOs) ameliorate diabetes-induced muscle atrophy. However, the systemic application of EXOs is less selective for diseased tissues, which reduces their efficacy and safety associated with their nonspecific biological distribution in vivo.
View Article and Find Full Text PDFhUC-MSC preserves erectile function by restoring mitochondrial mass of penile smooth muscle cells in a rat model of cavernous nerve injury via SIRT1/PGC-1a/TFAM signaling.
Biol Res
January 2025
Department of Urology and Andrology, Renji Hospital, Shanghai Institute of Andrology, School of Medicine, Shanghai Jiaotong University, Shanghai, 200127, China.
Background: Cavernous nerve injury-induced erectile dysfunction (CNI-ED) is a common complication following radical prostatectomy and severely affects patients' quality of life. The mitochondrial impairment in corpus cavernosum smooth muscle cells (CCSMCs) may be an important pathological mechanism of CNI-ED. Previous studies have shown that transplantation of human adipose derived stem cells (ADSC) can alleviate CNI-ED in a rat model.
View Article and Find Full Text PDFKdm2a inhibition in skeletal muscle improves metabolic flexibility in obesity.
Nat Metab
January 2025
Tongji Shanxi Hospital, Shanxi Bethune Hospital, Shanxi Academy of Medical Science, Third Hospital of Shanxi Medical University, the Key Laboratory of Endocrine and Metabolic Diseases of Shanxi Province, Taiyuan, China.
Skeletal muscle is a critical organ in maintaining homoeostasis against metabolic stress, and histone post-translational modifications are pivotal in those processes. However, the intricate nature of histone methylation in skeletal muscle and its impact on metabolic homoeostasis have yet to be elucidated. Here, we report that mitochondria-rich slow-twitch myofibers are characterized by significantly higher levels of H3K36me2 along with repressed expression of Kdm2a, an enzyme that specifically catalyses H3K36me2 demethylation.
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