Journal September 25, 2026 5 min read

How the mTOR Pathway Changes with Age

A research-supply overview of mTOR signalling in ageing, drawing on animal, in vitro and clinical-trial evidence. For laboratory research use only.

peptides-pro Editorial

What mTOR is

Mechanistic target of rapamycin (mTOR) is a serine/threonine protein kinase of the phosphatidylinositol 3-kinase-related kinase family. It is the catalytic subunit of two distinct complexes, mTORC1 and mTORC2, and is encoded in humans by the gene MTOR. The evidence block used for this page does not supply a sequence, formula or molecular weight for mTOR, so none is stated here.

The work described below centres on the PI3K/Akt/mTOR signalling axis and its upstream regulators PTEN and c-MET, together with the RhoA pathway that runs in parallel with mTOR in fibrotic tissue [1][4][6].

Research Studies

LL-37 and SQLE-mediated cholesterol synthesis via PTEN/AKT/mTOR in osteosarcoma cells

In osteosarcoma cell lines and normal human bone marrow mesenchymal stem cells, the human cathelicidin peptide LL-37 was reported to suppress SQLE-mediated cholesterol synthesis through the PTEN/AKT/mTOR pathway, with effects measured on viability, clonogenic survival, migration, invasion, cell-cycle distribution and cell death [1]. This is an in vitro finding in a cancer cell model and does not describe mTOR behaviour in healthy ageing tissue.

Intramuscular fat deposition and mTOR in Yanbian yellow cattle

In 60 24-month-old Yanbian yellow cattle (n = 30 per group), high- and low-intramuscular-fat groups were compared under standardised environmental and dietary conditions. Integrated transcriptomics and non-targeted metabolomics (n = 8 per group) associated intramuscular fat deposition with an upstream signalling layer comprising PPAR, PI3K-Akt and mTOR pathways, and a downstream metabolic execution layer [2]. This is a bovine production study, not an ageing study, and the animals were of a single age.

Fingolimod and RhoA/mTOR-driven interstitial expansion in kidney transplants

A randomised, double-blind, placebo-controlled trial in de novo kidney transplant recipients is testing whether adding fingolimod (FTY720) to standard immunosuppression prevents expansion of the interstitial compartment of the transplanted kidney. The stated hypothesis is that abrogating the fibrogenic effects of both the RhoA and mTOR pathways will reduce structural damage and possible subsequent transplant failure [4]. This is an ongoing clinical trial in transplant patients; no outcome data are reported in the evidence block.

Alpha ketoglutarate and postoperative systemic inflammatory response in colorectal surgery

The RISIS-CR trial proposes to identify inflammatory responsiveness in patients before colorectal cancer surgery and to give prophylactic anti-inflammatory treatment only to those with an excessive pro-inflammatory response. The proposal describes geroprotectors as reducing inflammation and potentially reducing postoperative systemic inflammatory response and complications, and names alpha ketoglutarate (AKG) as the geroprotector supplement to be used [3]. This is a registered trial protocol in a surgical population; it does not report mTOR measurements.

lncRNA DANCR and the miR-19a-3p/PTEN/AKT/mTOR axis in bone marrow mesenchymal stem cells

A study of osteogenic differentiation in bone marrow mesenchymal stem cells investigated the role of the long non-coding RNA DANCR and its targeting of the miR-19a-3p/PTEN/AKT/mTOR pathway in the context of osteoporosis [5]. This is a cell-level mechanistic study.

Anlotinib and c-MET/AKT/mTOR signalling in glioma cells

In human glioma cells, anlotinib was reported to inhibit proliferation, migration and invasion, with the effects examined for association with suppression of hepatocyte growth factor receptor (c-MET)/AKT/mTOR signalling and altered expression of autophagy-associated proteins [6]. This is an in vitro cancer study.

Pharmacological mTOR activation and trophectoderm differentiation in bovine embryos

In mice, the mTOR pathway influences the Hippo pathway and trophectoderm-related gene expression, but these mechanisms are not fully characterised in bovine embryos. Pharmacological activation of the mTOR pathway did not enhance trophectoderm differentiation in bovine embryos in the study examined [7]. This is an embryo model and is not informative about ageing in adult tissue.

Mitochondria-enriched BMSC exosomes and PI3K/Akt/mTOR in Parkinson's disease models

Mitochondrial dysfunction and neuroinflammation drive dopaminergic neuron loss in Parkinson's disease. Engineered mitochondrial-enriched small extracellular vesicles derived from bone marrow mesenchymal stem cells were studied for their capacity to restore microglia-neuron cross-talk, with PINK1/parkin and PI3K/Akt/mTOR pathways examined [8]. This is a disease-model study, not an ageing study.

Comparison of the models used

Evidence	Model or population	Pathway element examined
[1]	Osteosarcoma cell lines; normal human BMSCs (in vitro)	PTEN/AKT/mTOR
[2]	Yanbian yellow cattle, 24 months old	PPAR, PI3K-Akt, mTOR
[3]	Colorectal cancer surgery patients (trial protocol)	Inflammation; geroprotector AKG
[4]	De novo kidney transplant recipients (trial)	RhoA and mTOR
[5]	Bone marrow mesenchymal stem cells	miR-19a-3p/PTEN/AKT/mTOR
[6]	Human glioma cells (in vitro)	c-MET/AKT/mTOR
[7]	Bovine embryos	mTOR, Hippo
[8]	Parkinson's disease models	PINK1/parkin, PI3K/Akt/mTOR

If you are reading this for personal health reasons

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