MRTFA

2 papers4 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.

1 lab in 1 country

Funders: American Heart Association and 2 more

Animals1
Cells1

Effects

p38 MAPK signalling

upin mice1

1 study

MRTFA activates p38 MAPK signalling in mice.
“Mechanistically, a deficiency in MKL1 abolished AAA-induced p38 mitogen activated protein kinase (p38MAPK) activity.”
Animalsshown by MKL1 deficiency in AAA
MKL1 cooperates with p38MAPK to promote vascular senescence, inflammation, and abdominal aortic aneurysm
Redox biology20 Feb 2021

Associations

Aortic dissection

upin mice1

1 study

MRTFA raises the risk of aortic dissection in mice.
“Both gene deletion and pharmacological inhibition of MKL1 markedly protected mice from aortic dissection”
Animalsshown by gene deletion and pharmacological inhibition in Ang II-induced mice
MKL1 cooperates with p38MAPK to promote vascular senescence, inflammation, and abdominal aortic aneurysm
Redox biology20 Feb 2021