Longevity interventions modulate mechanotransduction and extracellular matrix (ECM) homeostasis in C. elegans. Aging is associated with changes in ECM composition, including collagen stiffening and reduced collagen expression. Longevity interventions slow age-related collagen stiffening and prolong the expression of collagens that are turned over. These prolonged collagen dynamics are mediated by a mechanical feedback loop involving hemidesmosome-containing structures that span from the exoskeletal ECM through the hypodermis, basement membrane ECM, to the muscles. This feedback loop couples mechanical forces to adjust ECM gene expression and longevity via the transcriptional co-activator YAP-1 across tissues. The study provides in-vivo evidence that coordinated ECM remodeling through mechanotransduction is required and sufficient to promote longevity. The ECM plays a crucial role in supporting cellular function and tissue integrity. It consists of various proteins, including collagens, glycoproteins, and proteoglycans, and provides mechanical support, stores growth factors, and regulates cellular homeostasis. Aging is characterized by alterations in ECM structure and function. In the absence of disease, a key signature of aging is the decline of collagen expression in skin, while collagen-rich basement membrane ECM increases 100-fold in humans during aging. Some collagens are synthesized early in life and remain in the ECM, while others are extensively remodeled and renewed within circadian rhythm. These changes in tissue-specific ECM compositions during aging have been documented using proteomics approaches. Changes in ECM composition have been implicated in numerous diseases, highlighting the importance of understanding the dynamic nature of the ECM. ECM composition can predict cancer types and adverse patient outcomes, and single-cell RNA sequencing data of ECM gene expression predicts cell type and development stage. Thus, ECM composition reflects cell identity, phenotypic state, health, or disease status. The concept of 'matreotype' is defined as a 'snapshot' of ECM composition associated with or caused by a phenotype or physiological state, such as health, disease, or age. Using RNA sequencing data, the youthful matreotype of humans has been defined, and several novel longevity drugs have been predicted and validated. Longevity-promoting interventions, both pharmacological and genetic, have been shown to influence ECM gene expression in C. elegans, mice, and humans. Using C. elegans, it has been shown that the effects of all so-far tested longevity interventions are abolished when non-essential collagens are knocked down during adulthood. This suggests that these collagens act downstream of diverse longevity interventions or function as a licensing signal for longevity. Conversely, overexpressing any of these three collagens is sufficient to increase C. elegans' lifespan. However, the underlying mechanism linking collagen remodeling to longevity remains unknown. The study monitors matreotypes (i.e., ECM composition) encompassing from expression to protein to incorporation and maintenance in the matrix in vivo during aging. It shows that certain cuticularLongevity interventions modulate mechanotransduction and extracellular matrix (ECM) homeostasis in C. elegans. Aging is associated with changes in ECM composition, including collagen stiffening and reduced collagen expression. Longevity interventions slow age-related collagen stiffening and prolong the expression of collagens that are turned over. These prolonged collagen dynamics are mediated by a mechanical feedback loop involving hemidesmosome-containing structures that span from the exoskeletal ECM through the hypodermis, basement membrane ECM, to the muscles. This feedback loop couples mechanical forces to adjust ECM gene expression and longevity via the transcriptional co-activator YAP-1 across tissues. The study provides in-vivo evidence that coordinated ECM remodeling through mechanotransduction is required and sufficient to promote longevity. The ECM plays a crucial role in supporting cellular function and tissue integrity. It consists of various proteins, including collagens, glycoproteins, and proteoglycans, and provides mechanical support, stores growth factors, and regulates cellular homeostasis. Aging is characterized by alterations in ECM structure and function. In the absence of disease, a key signature of aging is the decline of collagen expression in skin, while collagen-rich basement membrane ECM increases 100-fold in humans during aging. Some collagens are synthesized early in life and remain in the ECM, while others are extensively remodeled and renewed within circadian rhythm. These changes in tissue-specific ECM compositions during aging have been documented using proteomics approaches. Changes in ECM composition have been implicated in numerous diseases, highlighting the importance of understanding the dynamic nature of the ECM. ECM composition can predict cancer types and adverse patient outcomes, and single-cell RNA sequencing data of ECM gene expression predicts cell type and development stage. Thus, ECM composition reflects cell identity, phenotypic state, health, or disease status. The concept of 'matreotype' is defined as a 'snapshot' of ECM composition associated with or caused by a phenotype or physiological state, such as health, disease, or age. Using RNA sequencing data, the youthful matreotype of humans has been defined, and several novel longevity drugs have been predicted and validated. Longevity-promoting interventions, both pharmacological and genetic, have been shown to influence ECM gene expression in C. elegans, mice, and humans. Using C. elegans, it has been shown that the effects of all so-far tested longevity interventions are abolished when non-essential collagens are knocked down during adulthood. This suggests that these collagens act downstream of diverse longevity interventions or function as a licensing signal for longevity. Conversely, overexpressing any of these three collagens is sufficient to increase C. elegans' lifespan. However, the underlying mechanism linking collagen remodeling to longevity remains unknown. The study monitors matreotypes (i.e., ECM composition) encompassing from expression to protein to incorporation and maintenance in the matrix in vivo during aging. It shows that certain cuticular