-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
- Cosmetic Ingredient
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
Guided reading: Decreasing mitochondrial function can lead to aging, but interestingly, mild mitochondrial stress early in life, and the reactive oxygen produced by mitochondrials may extend life.
mitochondrials are the factory of energy metabolism and also affect and regulate human life expectancy.
the decline in mitochondrial function can lead to aging, but interestingly, mild mitochondrial stress early in life (the adaptive regulation of mitochondrial stimulation) and reactive oxygen (ROS) produced by mitochondrials may extend life.
triacetic acid cycle in the mitochondrials is the final metabolic path of the three nutrients (sugars, lipids, amino acids).
these nutrients are biooxidized to produce acetyl coenzyme A (CoA) and then enter the triacetic acid cycle for degradation, a process that is important for maintaining breathing and generating energy.
, what is the link between the metabolite acetyl coenzyme A and aging? A recent article published in ScienceAdvances entitled "NuRD mediatesmitochondrial stress-induced longevity via chromatin remodeling in response toacetyl-CoA level" reveals for the first time that the metabolite acetyl coenzyme A can affect the aging process by reshaping chromosomes.
Doi:10.1126/sciadv.abb2529 Specifically, the study found that acetyl coenzyme A (CoA) as a key signal of mitochondrials regulates aging.
because when CoA decreases, histone deacetylase complex (NuRD) is activated to process chromatin (chromosomal remodeling), which causes aging.
and when nutrients are added to restore acetyl coenzyme A levels, life expectancy is reversed.
findings provide an important basis for research to extend human life expectancy.
when certain changes put pressure on the mitochondrial, the mitochondrial experience initiates a mitochondrial non-folding protein reaction (UPRmt) to protect the body, a mechanism that can be used to maintain protein stability in the mitochondrial body.
transcription factor DVE-1 (protein factor assisting transcription) is necessary for embryonic development and mitochondrial morphology maintenance, and is also involved in UPRmt signal conduction.
, the team first analyzed the relationship between the important transcription factors DEVE-1 and NuRD complexes in the mitochondrial stress response pathline using immunosuppression and protein spectra.
results show that NuRD complexes play a specific role in regulating mitochondrial stress, which can also lead to the accumulation of NuRD complexes in the nucleus.
UPRmt signal transduction nuRD (partial screenshot) mitochondrial stress reaction in DVE-1 under the NuRD complex sub-base in the cell nucleus accumulation prior to the study found that mitochondrial stress can induce the beautiful hidden rod nematodes of the intestinal nucleus as a whole chromatin remodeling, and NuRD complex in the chromosomal remodeling plays a role.
, the team looked at the effects of changes in NuRD composition in wild and NuRD mutant animals on chromatin structure.
found that nuRD complex is necessary for chromosomal remodeling caused by mitochondrial stress.
, how does mitochondrial stress cause NuRD-induced chromatin remodeling? Next, the researchers looked at the effects of acetyl coenzyme A, a participant in important metabolic pathlines, on these metabolic signals and the relationship with NuRD-induced chromosomal remodeling, starting with major metabolic changes in mitochondrial stress.
results found that reducing the activity of mitochondrial electron transmission chains (ETC) affected mitochondrial respiration, resulting in a decrease in acetyl coenzyme A in participants in the triamlic acid cycle (TCA), leading to a decrease in histone acetylation and chromatin remodeling.
the effects of acetyl coenzyme A on chromatin structure and NuRD complexes (partial screenshots) during
mitochondrial stress have led researchers to think that since changes in acetyl coenzyme A can lead to chromatin remodeling, NuRD complexes are necessary for chromosomal remodeling caused by mitochondrial stress.
, what is the connection between acetyl coenzyme A and NuRD complexes? Next, the team found through a series of experiments that acetyl coenzyme A is a metabolic intermediate that regulates mitochondrial metabolism and the metaphysical genome through the NuRD complex in the beautiful crypto-rod worm.
the decrease of acetyl coenzyme A will lead to chromatin structure changes (partial screenshots) to summarize the above results, in a simple way, acetyl coenzyme A levels decreased, can be induced NuRD complex to regulate histone acetylation levels to reshape chromatin structure.
, how does this have something to do with aging? To examine the mechanisms by which acetyl coenzyme A affects aging, the researchers conducted an interesting experiment to restore acetyl coenzyme A levels by supplementing nutrition (citrate, acetic acid, acetone and glucose) to observe the effects of mitochondrial stress on animal life.
results are surprising: animals can regulate cellular metabolic changes and dietary nutrient input levels during development, thus forming chromatin structures that leave lasting metagenetic characteristics that ultimately determine the aging process.
Dietary nutrients affect mitochondrial stress-induced life expectancy In summary, the study found that mitochondrial stress can cause a decrease in acetyl coenzyme A, nuRD complex feel acetyl coenzyme A levels drop, will accumulate and reshape chromatin structure in the nuclei of the cell, thereby affecting life.
this effect can be appropriately intervened by supplementing nutrients, which provides a whole new way of thinking for the study of the use of nutrient metabolism to regulate the aging of the body.
references: s1 s nuRDmediates mitochondrial stress-induced longevity via chromatin remodeling inresponsetoacetyl-CoA level s2' A system RNAi identifieses a critical role for mitochondria in C.