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Study · Not a test of the peptide alone · 2022

1 result

The relationship between myodural bridges, hyperplasia of the suboccipital musculature, and intracranial pressure.

Li C, Yue C, Liu ZC, Gong J, Wei XS, Yang H, Gilmore C, Yu SB, Hack GD, Sui HJ

PloS one2 Sept 2022Cited by 19 (Europe PMC)

PMID36054096 (opens in a new tab)PMCIDPMC9439232 (opens in a new tab)DOI10.1371/journal.pone.0273193 (opens in a new tab)PepBankPUB-36054096
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Summary

During mammalian evolution, the Myodural Bridges (MDB) have been shown to be highly conserved anatomical structures. However, the putative physiological function of these structures remains unclear. The MDB functionally connects the suboccipital musculature to the cervical spinal dura mater, while passing through the posterior atlanto-occipital and atlanto-axial interspaces. MDB transmits the tensile forces generated by the suboccipital muscles to the cervical dura mater. Moreover, head movements have been shown to be an important contributor to human CSF circulation. In the present study, a 16-week administration of a Myostatin-specific inhibitor, ACE-031, was injected into the suboccipital musculature of rats to establish an experimental animal model of hyperplasia of the suboccipital musculature. Using an optic fiber pressure measurement instrument, the present authors observed a significant increase in intracranial pressure (ICP) while utilizing the hyperplasia model. In contrast, surgically severing the MDB connections resulted in a significant decrease in intracranial pressure. Thus, these results indicated that muscular activation of the MDB may affect CSF circulation, suggesting a potential functional role of the MDB, and providing a new research perspective on CSF dynamics.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone1

In this study, ACE-031 (ramatercept) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking ACE-031 (ramatercept).

  1. 01AnimalNot a test of ACE-031 (ramatercept) aloneAnimal study (in vivo)Mechanism

    In rats, intracranial pressure increased significantly in the ACE‑031-induced suboccipital hyperplasia model.

    In plain wordsIn rats, pressure inside the skull increased in the muscle enlargement model induced with ACE‑031.

    Peptide
    ACE-031 (ramatercept)
    Outcome
    IncreaseIntracranial pressure in hyperplasia model
    Study

    ratn: not reported in source

    ACE-031-induced suboccipital muscle hyperplasia
    Outcome group
    Cerebrospinal fluid dynamics · Nervous system and cognition

    Source sentences

    Summary
    Using an optic fiber pressure measurement instrument, the present authors observed a significant increase in intracranial pressure (ICP) while utilizing the hyperplasia model.
    1 context sentence
    Summary · context
    In the present study, a 16-week administration of a Myostatin-specific inhibitor, ACE-031, was injected into the suboccipital musculature of rats to establish an experimental animal model of hyperplasia of the suboccipital musculature.

    In this study, ACE-031 (ramatercept) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking ACE-031 (ramatercept).

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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