MIR-29

1. MIR-29 inhibits methylome remodeling in vertebrates cells.

   “Methylome analysis reveals a broader function: inhibition releases the miR-29 brake on remodelling, and mimic treatment reinforces it.”

   Cellsshown by inhibition and mimic treatment

   Blocking an RNA counters aging-related gene activity in cells

   bioRxiv·Oct 23, 2026Preprint

1. MIR-29 increases transcriptional aging in vertebrates cells.

   “miR-29 inhibition opposes transcriptional ageing, whereas mimics promote an older transcriptional state.”

   Cellsshown by inhibition and mimic treatment

   Blocking an RNA counters aging-related gene activity in cells

   bioRxiv·Oct 23, 2026Preprint

1. MIR-29 decreases trabecular bone mass in mice.

   “reducing cortical bone thickness and trabecular bone mass”

   Animalsin Prx1-positive MSCs

   Targeting miR-29 mitigates skeletal senescence and bolsters therapeutic potential of mesenchymal stromal cells

   Cell reports. Medicine·Aug 20, 2024

1. MIR-29 increases cellular senescence in mice.

   “Genetic overexpression of miR-29 in Prx1-positive MSCs significantly accelerates skeletal senescence”

   Animalsin Prx1-positive MSCs

   Targeting miR-29 mitigates skeletal senescence and bolsters therapeutic potential of mesenchymal stromal cells

   Cell reports. Medicine·Aug 20, 2024

More on Cellular senescence

1. MIR-29 induces global gene expression in killifish.

   “miR-29 triggers a global gene expression response that partially overlaps with that induced by aging”

   Animals

   MicroRNA miR-29 controls a compensatory response to limit neuronal iron accumulation during adult life and aging

   bioRxiv (Cold Spring Harbor Laboratory)·Mar 31, 2016Preprint

1. MIR-29 decreases brain iron accumulation in killifish.

   “Transgenic fish with knock-down of miR-29 show significant adult-onset up-regulation of IRP2 and its target TFR1 in neurons and display enhanced age-dependent accumulation of brain iron”

   Animalsshown by miR-29 knockdownbrain

   MicroRNA miR-29 controls a compensatory response to limit neuronal iron accumulation during adult life and aging

   bioRxiv (Cold Spring Harbor Laboratory)·Mar 31, 2016Preprint

1. MIR-29 decreases IRP2 expression in killifish.

   “Transgenic fish with knock-down of miR-29 show significant adult-onset up-regulation of IRP2 and its target TFR1 in neurons”

   Animalsshown by miR-29 knockdownneuron

   MicroRNA miR-29 controls a compensatory response to limit neuronal iron accumulation during adult life and aging

   bioRxiv (Cold Spring Harbor Laboratory)·Mar 31, 2016Preprint

More on IRP2 expression

1. MIR-29 is associated with age in vertebrates.

   “miR-29 rises with ageing, falls in both rejuvenation settings and shows the most conserved age-associated increase across vertebrates.”

   Review

   Blocking an RNA counters aging-related gene activity in cells

   bioRxiv·Oct 23, 2026Preprint