Peptide directoryBone, muscle & mineral

SPAR

A lysosomal micropeptide that holds back mTORC1 and slows muscle regeneration.

Where it comes from

Made in
Muscle and endothelium
Sent out by
Not secreted
Acts on
  • The v-ATPase and the mTORC1 amino acid sensor

What it does

  • Stops mTORC1 from switching on when amino acids arrive 1
  • Falls after muscle injury so regeneration can proceed; mice without it regenerate faster 1
  • Also reported to promote new blood vessels 2

In medicine

  • No medicine acts on it, no test measures it and no disease has been traced to its gene
  • Its clinical interest is borrowed from mTORC1, the switch it holds shut and that rapamycin and its analogues block from the other side

Beyond the body’s own use

  • Deleting it made injured mouse muscle regenerate faster, which is the whole case for lowering it in muscle wasting; it has never been tried in a person 1
  • The RNA and the peptide it carries do not do the same job: in blood-vessel cells they pulled endothelial function in opposite directions, so an experiment that removes both answers neither question 2
  • What is being asked next is whether the peptide can be lowered while the transcript is left alone, and whether lifting a brake on mTORC1 anywhere can be made safe

Sources

  1. Matsumoto et al., mTORC1 and muscle regeneration are regulated by the LINC00961-encoded SPAR polypeptide, Nature 2017
  2. Spencer et al., The LINC00961 transcript and its micropeptide regulate endothelial cell function, Cardiovascular Research 2020

This card describes what a medicine is for and what the evidence says; it recommends nothing. Talk to your clinician about anything you read here.