ARG2

4 papers8 findings

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

Labs are independent when their papers share no last author and no institution.

Against: findings that point the other way from most findings on the same outcome.

On aging: the drug’s trials ARN judged to be about aging, of every trial that tests it for any use.

No results posted: trials that ended more than a year ago with no results on ClinicalTrials.gov and no paper in ARN’s record.

Company ties: findings with an author at a company, or from a paper whose competing-interests statement declares ties to one.

A gene’s or a process’s line counts the gene with the processes named after it, as NLRP3 with the NLRP3 inflammasome, and the trials of drugs aimed at it.

2 independent labs in 2 countries

Funders: National Science Foundation and 7 more

Animals3
Cells1

Effects

NF-κB signalling

upin human cells1

1 study

ARG2 activates NF-κB signalling in human cells.
“Accumulation of ARG2 subsequently activates mTOR and NF-κB signaling and thereby establishes a robust SASP”
Cells
m¹A-Dependent TRMT6/61A-ARG2 Axis Drives Protumorigenic Senescence by Remodeling the Tumor Microenvironment
Advanced science (Weinheim, Baden-Wurttemberg, Germany)8 Jan 2026

Upstream

TRMT6/TRMT61ACOMPLEX

upin human cells1

1 study

TRMT6/TRMT61ACOMPLEX increases ARG2 in human cells.
“TRMT6/61A-dependent m1A deposition on specific tRNAs enhances the translational efficiency of their cognate codons. This codon-biased translational control selectively boosts the synthesis of ARG2.”
Cells
m¹A-Dependent TRMT6/61A-ARG2 Axis Drives Protumorigenic Senescence by Remodeling the Tumor Microenvironment
Advanced science (Weinheim, Baden-Wurttemberg, Germany)8 Jan 2026

Associations

Ischemic injury

upin mice1

1 study

ARG2 raises the risk of ischemic injury in mice.
“Mice with genetic deficiency of Arg2 (Arg2-/-) are protected from age-associated cardiac inflammation, myocyte apoptosis, interstitial and perivascular fibrosis, endothelial-mesenchymal transition (EndMT), and susceptibility to ischemic injury.”
Animalsshown by genetic deficiency (Arg2-/-)
Cell-autonomous and non-cell-autonomous effects of Arginase 2 on cardiac aging
eLife4 Nov 2025