The Effects of mTOR Inhibition on Cell Senescence and Cellular Function in Human Cardiac Progenitor Cells: Insights from the STAT3-PIM1 Axis – Experimental & Molecular Medicine
Introduction:
Cellular senescence is a state of irreversible growth arrest that occurs in response to various stressors, including DNA damage, telomere shortening, and oxidative stress. Senescent cells lose their ability to divide and function properly, leading to tissue dysfunction and aging. In the context of cardiac progenitor cells (CPCs), which are responsible for cardiac repair and regeneration, senescence can have detrimental effects on cardiac function. Therefore, understanding the mechanisms underlying CPC senescence and finding ways to prevent or reverse it is of great importance.
mTOR (mechanistic target of rapamycin) is a key regulator of cell growth, metabolism, and aging. It plays a crucial role in the control of cellular senescence by integrating various signals, including nutrient availability, energy status, and growth factors. Inhibition of mTOR has been shown to extend lifespan and delay age-related diseases in various organisms. However, the effects of mTOR inhibition on CPC senescence and cellular function remain poorly understood.
Insights from the STAT3-PIM1 Axis:
A recent study published in Experimental & Molecular Medicine investigated the effects of mTOR inhibition on CPC senescence and cellular function, focusing on the STAT3-PIM1 axis. STAT3 (signal transducer and activator of transcription 3) is a transcription factor that plays a critical role in cell survival, proliferation, and differentiation. PIM1 (proviral integration site for Moloney murine leukemia virus 1) is a serine/threonine kinase that regulates cell cycle progression and apoptosis.
The researchers first examined the expression levels of STAT3 and PIM1 in senescent CPCs. They found that both STAT3 and PIM1 were significantly downregulated in senescent CPCs compared to young CPCs. This suggests that the STAT3-PIM1 axis may be involved in CPC senescence.
Next, the researchers investigated the effects of mTOR inhibition on CPC senescence and cellular function. They treated senescent CPCs with rapamycin, a well-known mTOR inhibitor. They found that rapamycin treatment significantly increased the expression levels of STAT3 and PIM1 in senescent CPCs. Moreover, rapamycin treatment reduced senescence-associated markers and improved cellular function in senescent CPCs.
To further confirm the role of the STAT3-PIM1 axis in mediating the effects of mTOR inhibition, the researchers performed knockdown experiments. They knocked down STAT3 or PIM1 in senescent CPCs and treated them with rapamycin. They found that knockdown of either STAT3 or PIM1 abolished the beneficial effects of rapamycin on senescence and cellular function in CPCs.
Conclusion:
This study provides valuable insights into the effects of mTOR inhibition on CPC senescence and cellular function. The findings suggest that mTOR inhibition can reverse CPC senescence and improve cellular function through the activation of the STAT3-PIM1 axis. These findings have important implications for cardiac repair and regeneration, as targeting mTOR and its downstream effectors may be a potential therapeutic strategy for preventing or reversing cardiac aging and dysfunction.
Further research is needed to fully understand the molecular mechanisms underlying the effects of mTOR inhibition on CPC senescence and cellular function. Additionally, future studies should investigate the effects of mTOR inhibitors in animal models and clinical trials to validate their potential as therapeutic interventions for cardiac aging and disease.
- SEO Powered Content & PR Distribution. Get Amplified Today.
- PlatoData.Network Vertical Generative Ai. Empower Yourself. Access Here.
- PlatoAiStream. Web3 Intelligence. Knowledge Amplified. Access Here.
- PlatoESG. Carbon, CleanTech, Energy, Environment, Solar, Waste Management. Access Here.
- PlatoHealth. Biotech and Clinical Trials Intelligence. Access Here.
- Source: Plato Data Intelligence.
- Source Link: https://platohealth.ai/author-correction-pharmacological-inhibition-of-mtor-attenuates-replicative-cell-senescence-and-improves-cellular-function-via-regulating-the-stat3-pim1-axis-in-human-cardiac-progenitor-cells-exper/