Retro Bio, backed by Sam Altman, is chasing a 5 billion dollar valuation to use AI and cell reprogramming to add 10 healthy years to human life.
Peripheral nerves—the network connecting the brain, spinal cord, and central nervous system to the rest of the body—transmit sensory information, control muscle movements, and regulate automatic bodily functions. Bioelectronic devices implanted on these nerves offer remarkable potential for the treatment and rehabilitation of neurological and systemic diseases.
However, because the body perceives these implants as foreign objects, they often trigger the formation of dense fibrotic tissue at bioelectronic device–tissue interfaces, which can significantly compromise device performance and longevity.
COX7RP is a critical factor that assembles mitochondrial respiratory chain complexes into supercomplexes, which is considered to modulate energy production efficiency. Whether COX7RP contributes to metabolic homeostasis and lifespan remains elusive. We here observed that COX7RP-transgenic (COX7RP-Tg) mice exhibit a phenotype characterized by a significant extension of lifespan. In addition, metabolic alterations were observed in COX7RP-Tg mice, including lower blood glucose levels at 120 min during the glucose tolerance test (GTT) without a significant difference in the area under the curve (AUC), as well as reduced serum triglyceride (TG) and total cholesterol (TC) levels. Moreover, COX7RP-Tg mice exhibited elevated ATP and nicotinamide adenine dinucleotide levels, reduced ROS production, and decreased senescence-associated β-galactosidase levels. Single-nucleus RNA-sequencing (snRNA-seq) revealed that senescence-associated secretory phenotype genes were downregulated in old COX7RP-Tg white adipose tissue (WAT) compared with old WT WAT, particularly in adipocytes. This study provides a clue to the role of mitochondrial respiratory supercomplex assembly factor COX7RP in resistance to aging and longevity extension.
Yang, Jn-Simon, He et al. report that the dual BCL-xL/BCL-2 PROTAC 753b is a potent and liver-tropic senolytic, which (unlike other inhibitors of BCL-xL) does not cause severe thrombocytopenia. They evaluate its efficacy in natural aging and in reducing progression from steatotic liver disease to hepatocellular carcinoma, using mouse models.
One of the hallmarks of cancer cells is their ability to evade apoptosis, or programmed cell death, through changes in protein expression. Inducing apoptosis in cancer cells has become a major focus of novel cancer therapies, as these approaches may be less toxic to healthy tissue than conventional chemotherapy or radiation. Many chemical agents are currently being tested for their ability to trigger apoptosis, and researchers are increasingly exploring light-activated molecules that can be precisely targeted to tumor sites using lasers, sparing surrounding healthy tissue.
Cancer cells have mitochondria that supply energy for rapid growth and division, but an overly alkaline environment is thought to disrupt mitochondrial function, leading to apoptosis.
A microbial protein called Archaerhodopsin-3 (AR3) may hold the key to alkalinity-induced apoptosis. When exposed to green light, AR3 pumps hydrogen ions out of the cell, increasing alkalinity, disrupting cellular functions, and eventually inducing apoptosis.