Results 51 to 60 of about 9,936 (203)
Cells, 2023 Hutchinson–Gilford progeria syndrome (HGPS) is a rare genetic disease that causes premature aging symptoms, such as vascular diseases, lipodystrophy, loss of bone mineral density, and alopecia. HGPS is mostly linked to a heterozygous and de novo mutation
Ramona Hartinger +4 more
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Transmembrane Protein PTCHD4 Is a Novel Regulator of Cellular Senescence and Age‐Related Pathologies
Aging Cell, Volume 25, Issue 9, September 2026.PTCHD4 is induced by aging‐ and injury‐associated stresses and acts as a senescence‐associated transmembrane regulator. Through AKT activation, PTCHD4 promotes cellular senescence, SASP, functional decline, and pulmonary fibrosis, whereas PTCHD4 deficiency dampens AKT signaling and alleviates senescence‐associated pathological phenotypes.
Mingyue Wang +11 more
wiley +1 more source
Vascular smooth muscle cell loss underpins the accelerated atherosclerosis in Hutchinson-Gilford progeria syndrome [PDF]
, 2019 Lamin A, a product of the LMNA gene, is an essential nuclear envelope component in most differentiated cells. Mutations in LMNA have been linked to premature aging disorders, including Hutchinson-Gilford progeria syndrome (HGPS).
Hamczyk, Magda Rita +2 more
core +1 more source
Journal of Pediatric Neurosciences, 2013 Hutchinson-Gilford progeria syndrome (HGPS) is a very rare genetic disorder characterized by premature ageing, severe growth failure, and very early onset atherosclerosis.
Upendra Hansda +3 more
doaj +1 more source
Proteostasis of organelles in aging and disease
The FEBS Journal, Volume 293, Issue 18, Page 5600-5626, September 2026.Cells rely on regulated proteostasis mechanisms to keep their internal compartments functioning properly. When these mechanisms fail, damaged proteins accumulate, disrupting organelles, such as the nucleus, mitochondria, endoplasmic reticulum, Golgi, and lysosomes, as well as membraneless organelles, such as stress granules, processing bodies, the ...
Yara Nabawi +5 more
wiley +1 more source
Aging Cell, Volume 25, Issue 8, August 2026.Skeletal muscle aging is associated with a decrease in expression of the lactate receptor GPR81. Treating senescent myoblasts in vitro and progeric mice in vivo with GPR81 agonist decreases intramyocellular lipid accumulation and reverses hallmarks of aging. ABSTRACT Skeletal muscle aging is associated with increased lipid accumulation, or myosteatosis,
Pihu Mehrotra +11 more
wiley +1 more source
Progeroid Syndrome and Mutation in LMNA Gene: Report of Two Cases from Iran [PDF]
Journal of Kerman University of Medical Sciences, 2005 Two Iranian cases with very rare progeroid syndrome are reported. The first is a 24-year-old girl who has been healthy till her 13th birthday. From that time she has been suffering from a progressive generalized and multi-systemic illness.
Y Shafeghati, N Levy, G.M Martin
doaj
The telomeric protein AKTIP interacts with A- and B-type lamins and is involved in regulation of cellular senescence [PDF]
Open Biology, 2016 AKTIP is a shelterin-interacting protein required for replication of telomeric DNA. Here, we show that AKTIP biochemically interacts with A- and B-type lamins and affects lamin A, but not lamin C or B, expression.
Romina Burla +14 more
doaj +1 more source
Indian journal of dermatology, venereology and leprology, 2012 A case of progeria is being reported in a 7-year old boy. He had characteristic facies, short stature, alopecia, high pitched voice, coxa valga and sclerodermatous changes in skin.
C, Kaur +3 more
openaire +3 more sources
Frontiers in Cell and Developmental Biology, 2019 Emerin (EMD) and barrier to autointegration factor 1 (BANF1) each bind A-type lamins (LMNA) as fundamental components of nuclear lamina structure. Mutations in LMNA, EMD and BANF1 are genetically linked to many tissue-specific disorders including Emery ...
Tejas Dharmaraj +5 more
doaj +1 more source