Publications by authors named "Alessandro Giovanni Cerchiara"
Article Synopsis
- Myogenesis, the process of forming and regenerating skeletal muscle, can be significantly disrupted in Duchenne muscular dystrophy (DMD) due to lack of dystrophin, a key cytoskeletal protein.
- Research involved comparing two types of mouse muscle cell lines, one normal (wild-type) and one dystrophic, to analyze changes in ion channel activity and gene expression during muscle differentiation.
- Findings showed increased inward current density and altered gene expression in dystrophic cells, suggesting that ion channels could be potential targets for treatment and biomarkers for monitoring muscle development in DMD.
The potential role of liver kinase B1 (LKB1) in the altered activation of the master metabolic and epigenetic regulator adenosine monophosphate-activated protein kinase (AMPK) in Duchenne muscular dystrophy has not been investigated so far. Hence, we analyzed both gene and protein levels of LKB1 and its related targets in gastrocnemius muscles of adult C57BL/10 mdx mice and D2 mdx mice, a model with a more severe dystrophic phenotype, as well as the sensitivity of the LKB1-AMPK pathway to AMPK activators, such as chronic exercise. Our data show, for the first time, a reduction in the levels of LKB1 and accessory proteins, MO25 and STRADα, in both mdx strains versus the respective wild type, which was further impaired by exercise, in parallel with a lack of further phosphorylation of AMPK.
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- Growth hormone secretagogues (GHSs) have multiple functions, including activating specific receptors and controlling inflammation and metabolism, which may be beneficial for treating Duchenne muscular dystrophy (DMD).
- In a study with mice, two GHS compounds, EP80317 and JMV2894, showed improved muscle strength and reduced fibrosis when administered over eight weeks.
- Both treatments led to positive changes in muscle metabolism and gene expression, indicating potential new mechanisms for muscle recovery that do not rely on traditional pathways like IGF-1.
Article Synopsis
- Voltage-gated sodium channels are key targets for drug discovery due to their role in various physiological processes and disorders like epilepsy and chronic pain.
- In particular, myotonia is a condition that causes muscle stiffness from over-excitability of muscle fibers, and existing treatments include sodium channel blockers like mexiletine.
- The text emphasizes the need for more specific and effective drugs targeting the Na1.4 sodium channel isoform and discusses research on new compounds that may help treat myotonia.