Aging-Related Changes in Inflammatory and LKB1/AMPK Gene Expression in Fibromyalgia Patients

Abstract

Aging is characterized by a progressive loss of physiological integrity, leading to the impairment of numerous functions and increased vulnerability to death. This deterioration is the primary risk factor for aging‐related major human pathologies, including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases 1. Several interconnected molecular events are involved in this process. Efficient control of energy metabolic homeostasis, enhanced stress resistance, and qualified cellular housekeeping are the hallmarks of improved health span and extended lifespan. Adenosine monophosphate‐activated protein kinase (AMPK), the master regulator of cell energy levels, is activated by low adenosine triphosphate (ATP) levels that, in turn, increases glucose transport, fatty acid oxidation, and mitochondrial biogenesis. Furthermore, AMPK is also involved in the control of inflammatory processes 2. Recent studies also indicate that the sensitivity of AMPK to cellular stress declines with aging, and this could impair downstream signaling and the maintenance of cellular energy balance and stress resistance. AMPK signaling decline can also decrease mitochondrial biogenesis, increase cellular stress, and induce inflammation, which are typical events of the aging process