KMT2D

2 papers3 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 2 countries

Funders: Amgen and 1 more

Cells1

Effects

Chondrocyte hypertrophy

downin cells1

1 study

KMT2D decreases chondrocyte hypertrophy in cells.
“These findings demonstrate that KMT2D loss induces oxidative stress-driven chondrocyte hypertrophy, disrupting the balance of cartilage growth and ossification.”
CellsShown by KMT2D losschondrocyte
Loss of KMT2D accelerates hypertrophic chondrocyte differentiation and senescence by increasing mitochondrial ROS production
bioRxiv (Cold Spring Harbor Laboratory)19 Mar 2026Preprint

Cellular senescence

downin cells1

1 study

KMT2D inhibits cellular senescence in cells.
“KMT2D-deficient chondrocytes exhibit accelerated differentiation and early senescence upon exposure to supraphysiological oxygen levels (20% O2).”
CellsShown by KMT2D deficiency under supraphysiological oxygenchondrocyte20% O2
Loss of KMT2D accelerates hypertrophic chondrocyte differentiation and senescence by increasing mitochondrial ROS production
bioRxiv (Cold Spring Harbor Laboratory)19 Mar 2026Preprint