HDAC9

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 1 country

Funders: Division of Graduate Education and 1 more

Humans1
Cells1

Effects

Senescence-associated secretory phenotype (SASP)

upin human cells1

1 study

HDAC9 induces senescence-associated secretory phenotype (SASP) in human cells.
“HDAC9 upregulation in high-glucose-stimulated HK-2 cells was accompanied by mitochondrial impairment and increased levels of p53, p21, p16, and senescence associated secretory phenotype (SASP) factors.”
Cellshigh-glucose stimulation in HK-2 cells
Integrative transcriptomic and machine learning analyses identify HDAC9 as a key regulator of mitochondrial dysfunction and senescence-associated inflammation in diabetic nephropathy
Frontiers in immunology29 Aug 2025

More on Senescence-associated secretory phenotype (SASP)

Cellular senescence

upin human cells1

1 study

HDAC9 induces cellular senescence in human cells.
“HDAC9 upregulation in high-glucose-stimulated HK-2 cells was accompanied by mitochondrial impairment and increased levels of p53, p21, p16, and senescence associated secretory phenotype (SASP) factors.”
Cellshigh-glucose stimulation in HK-2 cells
Integrative transcriptomic and machine learning analyses identify HDAC9 as a key regulator of mitochondrial dysfunction and senescence-associated inflammation in diabetic nephropathy
Frontiers in immunology29 Aug 2025