Is REDD1 a metabolic double agent? Lessons from physiology and pathology

Area of Science:

• Cellular metabolism
• Molecular signaling pathways

Background:

• The Akt/mechanistic target of rapamycin (mTOR) pathway regulates cell growth and metabolism.
• Regulated in development and DNA damage response 1 (REDD1) is an endogenous inhibitor of Akt/mTOR signaling.
• REDD1 influences cell growth, mitochondrial function, oxidative stress, and apoptosis.

Purpose of the Study:

• To review the dual role of REDD1 in metabolic adaptation and disease pathogenesis.
• To explore the mechanisms underlying REDD1's context-dependent functions.
• To discuss the interplay between REDD1, Akt/mTOR signaling, and energy metabolism.

Main Methods:

• Literature review of studies on REDD1 function and regulation.
• Analysis of REDD1's role in various physiological and pathological conditions.
• Discussion of molecular mechanisms linking REDD1 to metabolic stress and disease.

Main Results:

• Transient REDD1 expression promotes energy conservation during metabolic stress, preventing energy collapse.
• Chronic REDD1 expression is associated with pathologies like inflammation, cancer, neurodegeneration, diabetes, and obesity.
• Prolonged REDD1 upregulation contributes to apoptosis, oxidative stress, and inflammation.

Conclusions:

• REDD1 acts as a metabolic double agent, with its effects dependent on expression duration.
• Understanding REDD1's dual role is crucial for developing therapeutic strategies for metabolic and inflammatory diseases.
• REDD1 is a key player in the cross-talk between Akt/mTOR signaling and cellular energy metabolism.