ReviewThe Journal of membrane biology2012
Connexin- and pannexin-based channels in normal skeletal muscles and their possible role in muscle atrophy.
Review in The Journal of membrane biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 37 citations in OpenAlex.
- The Unexplored Role of Connexin Hemichannels in Promoting Facioscapulohumeral Muscular Dystrophy Progression.International journal of molecular sciences · 2025Review
- Assessing the impact of boldine on the gastrocnemius using multiomics profiling at 7 and 28 days post-complete spinal cord injury in young male mice.Physiological genomics · 2023Article
- Orally administered boldine reduces muscle atrophy and promotes neuromuscular recovery in a rodent model of delayed nerve repair.Frontiers in cellular neuroscience · 2023Article
- CaNeuroscience letters · 2021Review
- Abnormal Calcium Handling in Duchenne Muscular Dystrophy: Mechanisms and Potential Therapies.Frontiers in physiology · 2021Review
- Pannexin 1 Regulates Skeletal Muscle Regeneration by Promoting Bleb-Based Myoblast Migration and Fusion Through a Novel Lipid Based Signaling Mechanism.Frontiers in cell and developmental biology · 2021Article
- eATP/P2X7R Axis: An Orchestrated Pathway Triggering Inflammasome Activation in Muscle Diseases.International journal of molecular sciences · 2020Review
- Connexin 43 Hemichannel Activity Promoted by Pro-Inflammatory Cytokines and High Glucose Alters Endothelial Cell Function.Frontiers in immunology · 2018Article
- The two faces of pannexins: new roles in inflammation and repair.Journal of inflammation research · 2018Review
- Connexins and Pannexins in Bone and Skeletal Muscle.Current osteoporosis reports · 2017Review
- Single-cell Microinjection for Cell Communication Analysis.Journal of visualized experiments : JoVE · 2017Article
- Pannexin 1 Modulates Axonal Growth in Mouse Peripheral Nerves.Frontiers in cellular neuroscience · 2017Article
- Fast skeletal myofibers of mdx mouse, model of Duchenne muscular dystrophy, express connexin hemichannels that lead to apoptosis.Cellular and molecular life sciences : CMLS · 2016Article
- Role of connexins and pannexins during ontogeny, regeneration, and pathologies of bone.BMC cell biology · 2016Review
- The absence of dysferlin induces the expression of functional connexin-based hemichannels in human myotubes.BMC cell biology · 2016Article
- Regulation of pannexin and connexin channels and their functional role in skeletal muscles.Cellular and molecular life sciences : CMLS · 2015Review
- The pannexins: past and present.Frontiers in physiology · 2014Review
- The role of pannexin hemichannels in inflammation and regeneration.Frontiers in physiology · 2014Review
- Pannexin 1 channels in skeletal muscles.Frontiers in physiology · 2014Article
- Antibodies targeting extracellular domain of connexins for studies of hemichannels.Neuropharmacology · 2013Review
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Precursor cells of skeletal muscles express connexins 39, 43 and 45 and pannexin1. In these cells, most connexins form two types of membrane channels, gap junction channels and hemichannels, whereas pannexin1 forms only hemichannels. All these channels are low-resistance pathways permeable to ions and small molecules that coordinate developmental events. During late stages of skeletal muscle differentiation, myofibers become innervated and stop expressing connexins but still express pannexin1 hemichannels that are potential pathways for the ATP release required for potentiation of the contraction response. Adult injured muscles undergo regeneration, and connexins are reexpressed and form membrane channels. In vivo, connexin reexpression occurs in undifferentiated cells that form new myofibers, favoring the healing process of injured muscle. However, differentiated myofibers maintained in culture for 48 h or treated with proinflammatory cytokines for less than 3 h also reexpress connexins and only form functional hemichannels at the cell surface. We propose that opening of these hemichannels contributes to drastic changes in electrochemical gradients, including reduction of membrane potential, increases in intracellular free Ca(2+) concentration and release of diverse metabolites (e.g., NAD(+) and ATP) to the extracellular milieu, contributing to multiple metabolic and physiologic alterations that characterize muscles undergoing atrophy in several acquired and genetic human diseases. Consequently, inhibition of connexin hemichannels expressed by injured or denervated skeletal muscles might reduce or prevent deleterious changes triggered by conditions that promote muscle atrophy.
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.