Increasing Collagen Slows Down Aging During Global Warming

Thermodynamic process controlled by the nervous system may extend the human lifespan as temperatures rise during the global warming era.

Identifying specific molecules and cells that affect the longevity response to temperature in nematode worms C. elegans, indicate that the inverse effects of temperature on longevity are not regulated simply by the thermodynamic process.

Studies in diverse species have found that higher temperatures are associated with a shorter lifespan and lower temperatures with a longer lifespan using the rate of living theory, based on the fact that higher temperatures increase chemical reaction rates, thus speeding up the aging process.

How Body Temperature Influences Ageing and Longevity

New research published in the journal Aging Cell suggests that this phenomenon is tied to a protein found in the nervous system that controls the expression of collagens, the primary building block of skin, bone, and connective tissue in many animals.

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Since the C. elegans’ protein is similar to nervous system receptor proteins found in other species including humans, the discovery potentially brings scientists closer to finding ways to harness collagen expression to slow down human aging and increase lifespan amid global warming.

Researchers looked at a nervous system protein known as NPR-8 in the tiny soil-dwelling worm Caenorhabditis elegans (C. elegans), a commonly used model organism in aging research. During their study, they observed that worms lacking NPR-8 had fewer skin wrinkles as they aged.

They also made the unexpected discovery that mutant worms kept at a warm temperature of 25 C (77 F) had increased collagen expression and lived longer than wild-type worms, which did not happen when the worms were kept at 20 C or 15 C (68 F and 59 F, respectively).

Longevity Response to Warm Temperature is Controlled via Collagen Genes

To determine whether the neural regulation of collagens may play a role in aging and longevity, they conducted a series of additional experiments and analyses. In one experiment, they reintroduced NPR-8 in mutant worms kept at 25 C and saw that this reverted the worms’ skin from smooth to wrinkled and significantly reduced the animals’ extended lifespan.

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Next, they showed that the extended lifespan of npr-8 mutant worms also held up under heat stress conditions, with mutant worms surviving significantly longer than wild-type worms when moved into a 35 C (95 F) environment.

Additional experiments identified specific neurons responsible for regulating lifespan in response to warm temperatures and pointed to increased expression of collagens as a driver of the improved lifespan at warm temperatures.

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The phenomenon of heat shortening lifespan has traditionally been explained by the rate of living theory, which suggests that heat speeds up an organism’s metabolism, causing it to use up its finite store of metabolic energy more quickly.

While the researchers still found limited evidence supporting this idea, their study findings indicate that the nervous system also plays an active role in this process.

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Given earlier findings that showed that worms lacking NPR-8 were more resistant to infection and oxidative stress, the researchers believe that the NPR-8-controlled increase in collagen expression boosts the animals’ resistance to stressful conditions such as excessive heat.

Their next step is to delve deeper into the underlying mechanisms of how increased collagen production enhances stress resistance. These findings also mean that down the road, it may be possible to intervene in that process to extend human lifespan as temperatures rise.

Source-Eurekalert