Abstract

While modernization has dramatically increased lifespan, it has also witnessed that the nature of stress has changed dramatically. Chronic stress result failures of homeostasis thus lead to various diseases such as atherosclerosis, non-alcoholic fatty liver disease (NAFLD) and depression. However, while 75%–90% of human diseases is related to the activation of stress system, the common pathways between stress exposure and pathophysiological processes underlying disease is still debatable. Chronic inflammation is an essential component of chronic diseases. Additionally, accumulating evidence suggested that excessive inflammation plays critical roles in the pathophysiology of the stress-related diseases, yet the basis for this connection is not fully understood. Here we discuss the role of inflammation in stress-induced diseases and suggest a common pathway for stress-related diseases that is based on chronic mild inflammation. This framework highlights the fundamental impact of inflammation mechanisms and provides a new perspective on the prevention and treatment of stress-related diseases.

Highlights

  • Stress is a state of threatened homeostasis provoked by a psychological, environmental, or physiological stressor

  • Elevated pro-inflammatory cytokines, increased microglia activation and accumulation of peripherally-derived monocytes and macrophages were detected in the brain with psychological stress exposure (Johnson et al, 2005)

  • While the biological mechanisms of stress increasing CVD risk are not well-known, chronic low-grade inflammatory load may emerge as a possible link as it is both elevated by chronic stress and contributed to early process, progression and thrombotic complications of atherosclerosis

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Summary

Introduction

Stress is a state of threatened homeostasis provoked by a psychological, environmental, or physiological stressor. Elevated pro-inflammatory cytokines, increased microglia activation and accumulation of peripherally-derived monocytes and macrophages were detected in the brain with psychological stress exposure (Johnson et al, 2005). By far, increasing literatures have shown that excessive inflammation play critical roles in the progression, and/or onset of stress-related diseases.

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