ReviewAmerican journal of physiology. Cell physiology2019
Diaphragm contractile weakness due to reduced mechanical loading: role of titin.
Review in American journal of physiology. Cell physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 31 citations in OpenAlex.
- The titin N2A-MARP signalosome constrains muscle longitudinal hypertrophy in response to stretch.eLife · 2026Article
- Glycerol storage increases passive stiffness of muscle fibers through effects on titin extensibility.The Journal of general physiology · 2025Article
- Intraoperative phrenic nerve stimulation to prevent diaphragm fiber weakness during thoracic surgery.PloS one · 2025Article
- Quantitative assessment of pneumothorax by using Shannon entropy of lung ultrasound M-mode image and diaphragmatic excursion based on automated measurement.Quantitative imaging in medicine and surgery · 2024Article
- Post-Myocardial Infarction Rehabilitation: The Absence in the Rehabilitation Process of the Diaphragm Muscle.International journal of general medicine · 2024Review
- Intracellular remodeling associated with endoplasmic reticulum stress modifies biomechanical compliance of bladder cells.Cell communication and signaling : CCS · 2023Article
- Rbm20International journal of molecular sciences · 2022Article
- Biomimetic Hydrogels in the Study of Cancer Mechanobiology: Overview, Biomedical Applications, and Future Perspectives.Gels (Basel, Switzerland) · 2022Review
- Unraveling the mysteries of the titin-N2A signalosome.The Journal of general physiology · 2021Article
- Titin N2A: More than a signaling node?The Journal of general physiology · 2021Article
- Muscle ankyrin repeat protein 1 (MARP1) locks titin to the sarcomeric thin filament and is a passive force regulator.The Journal of general physiology · 2021Article
- Urinary Titin N-Fragment as a Biomarker of Muscle Atrophy, Intensive Care Unit-Acquired Weakness, and Possible Application for Post-Intensive Care Syndrome.Journal of clinical medicine · 2021Review
- Single-Molecule Force Spectroscopy on the N2A Element of Titin: Effects of Phosphorylation and CARP.Frontiers in physiology · 2020Article
- Deleting Titin's C-Terminal PEVK Exons Increases Passive Stiffness, Alters Splicing, and Induces Cross-Sectional and Longitudinal Hypertrophy in Skeletal Muscle.Frontiers in physiology · 2020Article
- Effect of L-Arginine on Titin Expression in Rat Soleus Muscle After Hindlimb Unloading.Frontiers in physiology · 2019Article
- Molecular Mechanisms of Muscle Tone Impairment under Conditions of Real and Simulated Space Flight.Acta naturaeArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The diaphragm, the main muscle of inspiration, is constantly subjected to mechanical loading. Only during controlled mechanical ventilation, as occurs during thoracic surgery and in the intensive care unit, is mechanical loading of the diaphragm arrested. Animal studies indicate that the diaphragm is highly sensitive to unloading, causing rapid muscle fiber atrophy and contractile weakness; unloading-induced diaphragm atrophy and contractile weakness have been suggested to contribute to the difficulties in weaning patients from ventilator support. The molecular triggers that initiate the rapid unloading atrophy of the diaphragm are not well understood, although proteolytic pathways and oxidative signaling have been shown to be involved. Mechanical stress is known to play an important role in the maintenance of muscle mass. Within the muscle's sarcomere, titin is considered to play an important role in the stress-response machinery. Titin is a giant protein that acts as a mechanosensor regulating muscle protein expression in a sarcomere strain-dependent fashion. Thus titin is an attractive candidate for sensing the sudden mechanical arrest of the diaphragm when patients are mechanically ventilated, leading to changes in muscle protein expression. Here, we provide a novel perspective on how titin and its biomechanical sensing and signaling might be involved in the development of mechanical unloading-induced diaphragm weakness.
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.