Tier 4 — mechanistic

mTORC1 amplifies the ATF4-dependent de novo serine-glycine pathway to supply glycine during TGF-β 1 -induced collagen biosynthesis

Selvarajah B, Azuelos I, Platé M, Guillotin D, Forty EJ, Contento G, Woodcock HV, Redding M, Taylor A, Brunori G, Durrenberger PF, Ronzoni R, Blanchard AD, Mercer PF, Anastasiou D, Chambers RC
Science signaling 2019 12(582):eaav3048

Bibliography

PubMed
PMID 31113850
PubMed Central
PMC6584619
DOI
10.1126/scisignal.aav3048
Funding
Indexed support: Biotechnology and Biological Research Council; National Institute for Health Research (NIHR); Wellcome Trust; Biotechnology and Biological Sciences Research Council; Medical Research Council; Fonds de la Recherche en Santé – Québec; GlaxoSmithKline. See the publication for grant and funder details.
Competing interests
The accessible abstract does not establish the authors' competing interests; absence of a statement is not evidence of no conflicts.

Study snapshot

DesignLaboratory mechanistic study
ModelFibroblast cell models of TGF-beta1-stimulated collagen production
SampleFibroblast and pathway-perturbation experiments; n varies by assay
InterventionTGF-beta1 signaling with mTORC1/ATF4 and serine-glycine pathway manipulation
DurationIn-vitro mechanistic experiments
EndpointsDe novo glycine synthesis; Collagen production; mTORC1/ATF4 signaling

What the study showed, in plain terms

This paper explains how fibroblasts can increase internal glycine production during stimulated collagen synthesis. It is relevant to both tissue repair and fibrosis biology.

Key findings

  • mTORC1/ATF4 signaling supported the serine-glycine pathway during TGF-beta1 responses.
  • Changes in internal amino-acid synthesis influenced collagen output.

What this study can and cannot tell us

Internal metabolic pathway experiments are not oral supplementation tests.

More collagen is not automatically beneficial; fibrosis involves excessive collagen deposition.

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Editorial review

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Dr. Khaled Mahmoud, MBBChCritical Care Medicine, Longevity Science & Editorial Direction