The discovery of unforeseen data broadened the storyline beyond the singular function of a protein, extending it to include a more comprehensive mechanism. My most recent findings showing that PWP1 acts upstream of the Hedgehog pathway, and its role as a downstream element of the nutrient-sensing mTOR pathway, suggests PWP1 may serve as a molecular link between the mTOR and Hedgehog pathways in the nutrient-dependent regulation of intestinal homeostasis.
Early results from genetic manipulation experiments conducted on Drosophila, along with the use of Rapamycin to inhibit the mTOR pathway, revealed the activation of both PWP1 and Hedgehog, respectively. These findings seem to support the proposed hypothesis. Consequently, PWP1 is now positioned as a central player in a mechanism that extends beyond initial expectations, significantly enhancing the importance of my research in the scientific community.
The maintenance of tissue balance and overall organism health depends on the ability of stem cells to renew themselves and differentiate effectively. However, these features are gradually lost during aging, being the principal cause of the appearance of diseases and declining organ function. The resulting worsening of life quality also represents a substantial healthcare cost for society. Notably, nutrition plays a crucial role on the correct functioning of stem cells and therefore on tissue homeostasis and organismal health span. The access to a balanced diet and sufficient nutritional education is a privilege, which is not available for the entire human population. Advancing the current knowledge on nutrient regulation of tissue homeostasis will be a step forward in improving our understanding of the health effects of nutrition, with substantial societal relevance for the aging population. Hence, this research will have the potential of providing new insights on how the understanding of stem cell aging regulation in response to nutrient availability could ameliorate the process of both physiological and pathological tissue decline, with beneficial effects on health span.
