Perpetual Prompt ♾️, [08.05.2025 21:05]
631. Which extracellular matrix proteins (besides collagen and elastin) are most vulnerable to non-enzymatic glycation and critical for tissue functionality during aging?
632. How exactly does the extracellular matrix in various tissues of long-livers (naked mole rat, Greenland shark, giant turtles) differ from similar human tissues in terms of glycation resistance?
633. What specific mechanisms and enzymes ensure the removal or prevention of accumulation of advanced glycation end products (AGEs) in organisms with extreme longevity?
634. What is the role of ultra-high molecular weight hyaluronic acid in naked mole rat aging, and is it possible to genetically or pharmacologically transfer this phenotype to humans?
635. How does the structure and mechanical properties of the extracellular matrix of the jellyfish Turritopsis dohrnii change during reversion to a young state (polyp)?
636. What signaling pathways are involved in the immortal jellyfish for total remodeling of the extracellular matrix, and is it possible to transfer similar mechanisms to human cell cultures?
637. What are the molecular differences in the matrix between old and young human tissue that directly induce phenotypic aging of cells?
638. Is it possible to create a bioengineered extracellular matrix that is resistant to age-related damage by introducing unnatural amino acids or modifications that prevent cross-linking?
639. How do epigenetic markers of extracellular matrix aging influence the aging of adjacent cells?
640. How does glycated extracellular matrix affect the immune system and inflammation during human tissue aging?
641. What is the minimum degree of clearance of advanced glycation end products (AGEs) from the extracellular matrix required to fully restore youthful cellular behavior?
642. Which natural molecules (e.g., plant-derived) can effectively inhibit the formation of pathological cross-links in collagen and elastin?
643. Which microRNAs regulate the process of extracellular matrix remodeling in aging tissues, and can they be used to reverse aging?
644. How does age-related change in the composition of the extracellular matrix affect the ability of stem cells to regenerate tissue?
645. Which genes or molecular signaling cascades responsible for elastin synthesis in the aorta can be reactivated or supported to prevent atherosclerosis?
646. To what extent can restoration of aortic elasticity through the synthesis of new elastin reduce the overall biological load and prolong the functional life of the cardiovascular system?
647. What specific thymus-regulated immune factors are key regulators of extracellular matrix integrity and turnover?
648. How are blood sugar levels throughout a person's life related to the accumulation of pathological changes in the matrix of the heart, brain, and skin?
649. Can antidiabetic drugs (e.g., SGLT2 inhibitors or metformin) slow down matrix aging in healthy people without diabetes?
650. What is the dynamics of changes in extracellular matrix stiffness in different tissues depending on human age, and which tissues are most promising for primary intervention?
651. What is the influence of the gut microbiota and the metabolites it produces on the accumulation of AGE products in the extracellular matrix?
652. How can thymus rejuvenation and restoration of its activity affect the state of the extracellular matrix of peripheral tissues?
653. What are the mechanisms of extracellular matrix “detoxification” in young organisms and why do they weaken with age?
654. What transporters and receptors of cell membranes control the entry of glycated products into cells and can they become targets for anti-aging therapy?
655. How long-term is the effect of artificial renewal of the extracellular matrix and does it lead to compensatory negative consequences?
656. What effects does short-term stress or intermittent fasting have on slowing down the glycation of the extracellular matrix?
Perpetual Prompt ♾️, [08.05.2025 21:05]
657. What role does autophagy play in protecting the extracellular matrix from aging and is it possible to stimulate it to remove glycated proteins?
658. Which cell types (e.g. fibroblasts or macrophages) are most critical for controlling the structure and composition of the extracellular matrix in tissues?
659. Is there a point of no return in the accumulation of matrix damage, and is it possible to completely reverse these changes pharmacologically or bioengineeringly?
660. Which mathematical models and biomarkers of extracellular matrix health can be used to predict the remaining healthy life span of a person?