Progeria Latest Advances

The senescence-inhibitory p53 isoform Δ133p53α represses the proinflammatory chemokine CXCL10 in progeria model mice and naturally aged mice.

Journal: bioRxiv : the preprint server for biology

Published: April 10, 2026

STING causes replication stress and nascent DNA degradation via SAMHD1.

Journal: bioRxiv : the preprint server for biology

Published: April 03, 2026

Acetyl-CoA availability regulates neuronal metabolism, growth, and synaptic activity.

Journal: bioRxiv : the preprint server for biology

Published: February 06, 2026

Stem cell-associated osteogenic deficiency causes craniofacial deformities with progeroid accumulation of prelamin A.

Journal: JCI insight

Published: February 03, 2026

DNA-protein cross-links promote cGAS-STING-driven premature aging and embryonic lethality.

Journal: Science (New York, N.Y.)

Published: January 29, 2026

Craniofacial features associated with Hutchinson - Gilford progeria syndrome - A case report.

Journal: Stomatologija

Published: January 12, 2026

Senescence-inhibitory Δ133p53α counteracts accelerated ageing and mortality.

Journal: bioRxiv : the preprint server for biology

Published: January 09, 2026

Transcriptional profiling of Hutchinson-Gilford progeria patients identifies primary target pathways of progerin.

Journal: Nucleus (Austin, Tex.)

Published: January 05, 2026

Progeroid Syndrome with Signs of Autophagy Dysfunction in the Naked Mole Rat (Heterocephalus glaber).

Journal: Biochemistry. Biokhimiia

Published: December 26, 2025

Progerin expression in humans: implications for natural ageing.

Journal: Mechanisms of ageing and development

Published: December 09, 2025

Telomere dysfunction is associated with exacerbated intermittent hypoxia-induced cognitive deficits and nerve damage.

Journal: Frontiers in aging neuroscience

Published: December 02, 2025

Author Correction: p300 nucleocytoplasmic shuttling underlies mTORC1 hyperactivation in Hutchinson-Gilford progeria syndrome.

Journal: Nature cell biology

Published: November 29, 2025

Progeria Latest Advances

Find the Latest Research About Progeria

The senescence-inhibitory p53 isoform Δ133p53α represses the proinflammatory chemokine CXCL10 in progeria model mice and naturally aged mice.

The senescence-inhibitory p53 isoform Δ133p53α represses the proinflammatory chemokine CXCL10 in progeria model mice and naturally aged mice.

STING causes replication stress and nascent DNA degradation via SAMHD1.

STING causes replication stress and nascent DNA degradation via SAMHD1.

Acetyl-CoA availability regulates neuronal metabolism, growth, and synaptic activity.

Acetyl-CoA availability regulates neuronal metabolism, growth, and synaptic activity.

Stem cell-associated osteogenic deficiency causes craniofacial deformities with progeroid accumulation of prelamin A.

Stem cell-associated osteogenic deficiency causes craniofacial deformities with progeroid accumulation of prelamin A.

DNA-protein cross-links promote cGAS-STING-driven premature aging and embryonic lethality.

DNA-protein cross-links promote cGAS-STING-driven premature aging and embryonic lethality.

Craniofacial features associated with Hutchinson - Gilford progeria syndrome - A case report.

Craniofacial features associated with Hutchinson - Gilford progeria syndrome - A case report.

Senescence-inhibitory Δ133p53α counteracts accelerated ageing and mortality.

Senescence-inhibitory Δ133p53α counteracts accelerated ageing and mortality.

Transcriptional profiling of Hutchinson-Gilford progeria patients identifies primary target pathways of progerin.

Transcriptional profiling of Hutchinson-Gilford progeria patients identifies primary target pathways of progerin.

Progeroid Syndrome with Signs of Autophagy Dysfunction in the Naked Mole Rat (Heterocephalus glaber).

Progeroid Syndrome with Signs of Autophagy Dysfunction in the Naked Mole Rat (Heterocephalus glaber).

Progerin expression in humans: implications for natural ageing.

Progerin expression in humans: implications for natural ageing.

Telomere dysfunction is associated with exacerbated intermittent hypoxia-induced cognitive deficits and nerve damage.

Telomere dysfunction is associated with exacerbated intermittent hypoxia-induced cognitive deficits and nerve damage.

Author Correction: p300 nucleocytoplasmic shuttling underlies mTORC1 hyperactivation in Hutchinson-Gilford progeria syndrome.

Author Correction: p300 nucleocytoplasmic shuttling underlies mTORC1 hyperactivation in Hutchinson-Gilford progeria syndrome.