December 19, 2025
Blame it on the Gals
Timothy Birdnow
God punished Eve with bearing children and being stuck with an overbearing husband. I find this interesting as it suggests aging and sickness come through Eve, not Adam...
Mitochondria comes from the mother alone.
Scientists Found a New Way to Slow Aging Inside Cells
So the mitochondria is what makes us sickly and old. The article explains:
Balou the Bear told Mowgli in The Jungle Book (or at least the Disney version) "stay away from them, they're nothing but trouble". Seems the old bear knew more than we credited him..
God punished Eve with bearing children and being stuck with an overbearing husband. I find this interesting as it suggests aging and sickness come through Eve, not Adam...
Mitochondria comes from the mother alone.
Scientists Found a New Way to Slow Aging Inside Cells
Dec. 19, 2025 A small tweak to mitochondrial energy production led to big gains in health and longevity. Mice engineered to boost a protein that helps mitochondria work more efficiently lived longer and showed better metabolism, stronger muscles, and healthier ...
So the mitochondria is what makes us sickly and old. The article explains:
Inside mitochondria, energy production depends on respiratory chain complexes. These molecules move protons and electrons in ways that ultimately allow cells to make ATP. Researchers have known for years that these complexes can assemble into larger, flexible groupings called supercomplexes. These supercomplexes are thought to improve the efficiency of mitochondrial respiration.
Even so, solid evidence that directly connects supercomplexes to clear health benefits has been limited, especially from studies in animals. That gap has left an important question unresolved: do these structures actually make a measurable difference for aging and overall health?
The COX7RP protein under the microscope
To explore this, a team led by Team Leader Satoshi Inouefrom the Tokyo Metropolitan Institute for Geriatrics and Gerontology in Japan examined COX7RP, a mitochondrial protein that helps supercomplexes form. Their new study, co-authored by Dr. Kazuhiro Ikeda from Saitama Medical University in Japan, appeared in the journal Aging Cell.
"We previously identified COX7RP, a mitochondrial protein, as a key factor that promotes the formation of mitochondrial respiratory supercomplexes, thereby enhancing energy production and reducing reactive oxygen species (ROS) that cause oxidative stress in cells," explains Dr. Inoue. "Based on this, we investigated the role of COX7RP and mitochondrial respiratory supercomplexes in regulating aging and anti-aging processes."
Engineered mice lived longer and stayed healthier
The researchers created COX7RP-transgenic (COX7RP-Tg) mice that were designed to produce higher levels of COX7RP throughout their lives. With this model, the team could closely track how the protein affected lifespan, aging-related changes, and metabolism.
The results were striking. On average, the COX7RP-Tg mice lived 6.6% longer than wild-type mice. The benefits were not limited to lifespan alone, since the engineered mice also showed signs of better healthspan. They had improved glucose homeostasis due to greater insulin sensitivity, as well as improved lipid measures with lower blood triglycerides and total cholesterol. The team also found better muscle endurance and less fat buildup in the liver.
Stronger mitochondria and fewer aging signals
At the cellular level, the data pointed to a clear improvement in mitochondrial performance. In tissues from COX7RP-Tg mice, the formation of mitochondrial respiratory supercomplexes increased, and ATP production rose as well.
A closer look at white adipose tissue revealed shifts in multiple aging-related biomarkers. The mice showed higher levels of coenzyme NAD+, lower levels of ROS, and reduced levels of the cellular aging marker β-galactosidase. Using single-nucleus RNA sequencing on white adipose tissue from older mice, the researchers also found reduced activity in genes associated with age-related inflammation. This included genes tied to the senescence-associated secretory phenotype (SASP), a prototypic characteristic of senescent cells.
Even so, solid evidence that directly connects supercomplexes to clear health benefits has been limited, especially from studies in animals. That gap has left an important question unresolved: do these structures actually make a measurable difference for aging and overall health?
The COX7RP protein under the microscope
To explore this, a team led by Team Leader Satoshi Inouefrom the Tokyo Metropolitan Institute for Geriatrics and Gerontology in Japan examined COX7RP, a mitochondrial protein that helps supercomplexes form. Their new study, co-authored by Dr. Kazuhiro Ikeda from Saitama Medical University in Japan, appeared in the journal Aging Cell.
"We previously identified COX7RP, a mitochondrial protein, as a key factor that promotes the formation of mitochondrial respiratory supercomplexes, thereby enhancing energy production and reducing reactive oxygen species (ROS) that cause oxidative stress in cells," explains Dr. Inoue. "Based on this, we investigated the role of COX7RP and mitochondrial respiratory supercomplexes in regulating aging and anti-aging processes."
Engineered mice lived longer and stayed healthier
The researchers created COX7RP-transgenic (COX7RP-Tg) mice that were designed to produce higher levels of COX7RP throughout their lives. With this model, the team could closely track how the protein affected lifespan, aging-related changes, and metabolism.
The results were striking. On average, the COX7RP-Tg mice lived 6.6% longer than wild-type mice. The benefits were not limited to lifespan alone, since the engineered mice also showed signs of better healthspan. They had improved glucose homeostasis due to greater insulin sensitivity, as well as improved lipid measures with lower blood triglycerides and total cholesterol. The team also found better muscle endurance and less fat buildup in the liver.
Stronger mitochondria and fewer aging signals
At the cellular level, the data pointed to a clear improvement in mitochondrial performance. In tissues from COX7RP-Tg mice, the formation of mitochondrial respiratory supercomplexes increased, and ATP production rose as well.
A closer look at white adipose tissue revealed shifts in multiple aging-related biomarkers. The mice showed higher levels of coenzyme NAD+, lower levels of ROS, and reduced levels of the cellular aging marker β-galactosidase. Using single-nucleus RNA sequencing on white adipose tissue from older mice, the researchers also found reduced activity in genes associated with age-related inflammation. This included genes tied to the senescence-associated secretory phenotype (SASP), a prototypic characteristic of senescent cells.
Balou the Bear told Mowgli in The Jungle Book (or at least the Disney version) "stay away from them, they're nothing but trouble". Seems the old bear knew more than we credited him..
Posted by: Timothy Birdnow at
02:35 PM
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I remember reading The Jungle Book in my youth, and I could swear that Baloo was a Disney add-on, as I never remembered him from the Kipling original. And your quote, which is probably accurate, has the flavor of Disney but not of Kipling.
Posted by: Dana Mathewson at December 22, 2025 01:27 AM (XtojG)
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