ArticleJournal of muscle research and cell motility2007
Activation of caspase 3, 9, 12, and Bax in masseter muscle of mdx mice during necrosis.
Article in Journal of muscle research and cell motility, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Scutellarin alleviates liver injury in type 2 diabetic mellitus by suppressing hepatocyte apoptosisChinese herbal medicines · 2023Article
- Development and Regeneration of Muscle, Tendon, and Myotendinous Junctions in Striated Skeletal Muscle.International journal of molecular sciences · 2022Review
- Alteration of Oral and Perioral Soft Tissue in Mice following Incisor Tooth Extraction.International journal of molecular sciences · 2022Article
- Factors Involved in Morphogenesis in the Muscle-Tendon-Bone Complex.International journal of molecular sciences · 2021Review
- Mogroside IIe Ameliorates Cardiomyopathy by Suppressing Cardiomyocyte Apoptosis in a Type 2 Diabetic Model.Frontiers in pharmacology · 2021Article
- Article
- Caspase-12 ablation preserves muscle function in the mdx mouse.Human molecular genetics · 2014Article
- P38α MAPK underlies muscular dystrophy and myofiber death through a Bax-dependent mechanism.Human molecular genetics · 2014Article
- Article
- Apoptosis repressor with a CARD domain (ARC) restrains Bax-mediated pathogenesis in dystrophic skeletal muscle.PloS one · 2013Article
- Over-expression of BCL2 rescues muscle weakness in a mouse model of oculopharyngeal muscular dystrophy.Human molecular genetics · 2011Article
- Inhibition of prostaglandin D synthase suppresses muscular necrosis.The American journal of pathology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mdx mouse, a model of muscular dystrophy, lacks dystrophin, a cell membrane protein. It is known that the lack of dystrophin causes muscle fiber necrosis from 2 weeks after birth, and the majority of necrotic muscle fibers are replaced by regenerated muscle fibers by 4 weeks after birth. A recent study indicated the possibility that mitochondria-mediated intracellular stress, a phenomenon similar to apoptosis, may be produced during muscle fiber necrosis, but did not analyze endoplasmic reticulum-mediated intracellular stress. Therefore, we examined the expression of the caspase-12 gene involved in the endoplasmic reticulum stress pathway and the Bax, caspase-9, and caspase-3 genes involved in the mitochondrial stress pathway in the mdx masseter muscle. We found over-expression of caspase-12 in cells at 2-3 weeks after birth when muscle fiber necrosis was not prominent. This suggests that stress occurs in the endoplasmic reticulum to maintain cell morphology in the absence of dystrophin. In addition, Bax was abundantly expressed in the mdx masseter muscle at 3 weeks after birth, and the expression of caspase-9 and -3 was prominent at 3-4 weeks after birth when necrosis and regeneration were marked. These results indicate that endoplasmic reticulum and mitochondrial stresses are produced during necrosis of the mdx masseter muscle, and suggest that these events are a phenomenon similar to apoptosis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.