Key Highlights
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Fibro-adipogenic progenitor cells (FAPs) from the muscles of mice with spinal muscular atrophy (SMA) are inherently programmed to become fat cells, even when grown outside the body. This discovery reveals a muscle-intrinsic problem in SMA that persists after current therapies, explaining why patients still experience fat buildup and muscle weakness.
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The TIE2 receptor, not VEGFR2, is the critical link connecting two major signaling pathways that drive the formation of cerebral cavernous malformations (CCMs), which are vascular lesions in the brain. Blocking TIE2 activity almost completely prevented CCM formation in mouse models, suggesting it could be a promising new target for treating this disease in humans.
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Disease-causing mutations in human cardiac myosin alter the energy landscape of a key step called the “recovery stroke,” which prepares the protein to use energy from ATP. This disruption in the fundamental mechanics of the heart muscle protein helps explain how genetic mutations lead to cardiomyopathy and altered force generation.
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