Experiments using liver structures grown from high-fat-fed male rats found persistent changes resembling senescence, a state in which cells stop dividing.Experiments using liver structures grown from high-fat-fed male rats found persistent changes resembling senescence, a state in which cells stop dividing.
Experiments in liver organoids from male rats, against organoids from control-fed ratsMechanisms
Limit: Organoid cell composition was unknown; persistence was demonstrated in populations, not individual cells
In experiments, aged mice lacking the protein showed stronger age-linked brain cell activation, but no obvious loss of nerve insulation or faster decline in movement.In experiments, aged mice lacking the protein showed stronger age-linked brain cell activation, but no obvious loss of nerve insulation or faster decline in movement.
Experiments in adult and aged mice, against aged control miceMechanisms
Limit: The experiments did not distinguish adaptive activation from early, compensated persistent activation
Experiments using a human placental cell line also found reduced invasion into surrounding material when researchers increased the protein BCL10.Experiments using a human placental cell line also found reduced invasion into surrounding material when researchers increased the protein BCL10.
In a laboratory experiment, chemically induced senescent human retinal cells showed increased mobility and altered binding of proteins that anchor DNA to the nuclear…In a laboratory experiment, chemically induced senescent human retinal cells showed increased mobility and altered binding of proteins that anchor DNA to the nuclear scaffold.
In bone marrow stem cells linked to senile osteoporosis, lamin B1 loss triggered a form of cell death that disrupted mitochondria and impaired bone formation.In bone marrow stem cells linked to senile osteoporosis, lamin B1 loss triggered a form of cell death that disrupted mitochondria and impaired bone formation.
In mouse and human neurons, depleting POLK reduced repair-associated DNA synthesis and induced senescence-like stress, while augmenting POLK lowered DNA damage markers.In mouse and human neurons, depleting POLK reduced repair-associated DNA synthesis and induced senescence-like stress, while augmenting POLK lowered DNA damage markers.
Lipid nanoparticle delivery of base-editing mRNA restored DNA repair and heterochromatin structure in human neuromuscular models of premature aging.Lipid nanoparticle delivery of base-editing mRNA restored DNA repair and heterochromatin structure in human neuromuscular models of premature aging.
Vesicles from melatonin-treated stem cells targeted SRSF1 and SP1 to lower progerin and cellular prion protein in cell models.Vesicles from melatonin-treated stem cells targeted SRSF1 and SP1 to lower progerin and cellular prion protein in cell models.
In progeroid mice, activating the GPR81 receptor with the agonist CHBA reduced arterial lipid buildup, lowered cellular senescence, and improved endothelial integrity.In progeroid mice, activating the GPR81 receptor with the agonist CHBA reduced arterial lipid buildup, lowered cellular senescence, and improved endothelial integrity.