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glv126

Development of bio-impedance

**80**

**83**

**Chapter 5**

**Abstract**

for experiment research.

**1. Introduction**

Atrophy

Drugs for the Treatment of Muscle

Muscle mass is maintained through an interplay between anabolic and catabolic pathways. The ubiquitin-proteasome system plays an important role in the proteolysis progress during skeletal muscle atrophy which can be blocked by some proteasome inhibitors. But few studies have demonstrated the ability of these inhibitors to preserve muscle mass and architecture under catabolic condition in vivo. The insulin-like growth factor-1/phosphatidylinositide 3-kinases/protein kinase B/ mammalian target of rapamycin (IGF-1/PI3K/Akt/mTOR) pathway was associated with anabolic pathways. The activation of IGF-1 causes muscle hypertrophy; however, it cannot be used as a drug target. Myostatin pathway maintains activation that can induce skeletal muscle atrophy involved with various transcriptional and genetic factors. Skeletal muscle atrophy is a debilitating consequence of multiple chronic diseases and conditions that involve starvation. It reduces treatment options and positive clinical outcomes as well as compromising quality of life and increasing morbidity and mortality. Though considerable research has been undertaken to find the drug target and the molecular mechanisms that improve skeletal muscle atrophy, no drug was approved to treat skeletal muscle atrophy. However, these years, the signaling pathways involved in muscle atrophy were clarified and some effective treatments were currently available to prevent, attenuate, or reverse muscle atrophy

**Keywords:** muscle atrophy, sarcopenia, cachexia, anabolic, catabolic

The pathophysiology of skeletal muscle atrophy is multifactorial, with cancer, sepsis, renal and cardiac failure, acquired immune deficiency syndrome (AIDS) and chronic obstructive pulmonary disease (COPD) as well as inactivity or during aging [1–3]. These factors gradually lead to muscle wasting and weakness by decreasing protein synthesis and accelerating protein degradation, which are characterized by substantial decrease in myonuclear number, muscle fiber cross-sectional area, muscle strength and protein content while increasing in fatigability and resistance to insulin [4, 5]. Muscle atrophy is recognized as an independent predictor of mortality and is associated with functional impairment and poor quality of life [6]. Studies have revealed that different types of molecular mediators/catabolic players such as pro-inflammatory cytokines i.e. tumor necrosis factor-α (TNFα), interleukin-6 (IL-6), interleukin-1 (IL-1), interferon gamma (IFN-γ) and

*Linlin Chen, Hong Zhang, Mengyi Chi,* 

*Quanjun Yang and Cheng Guo*

**Chapter 5**
