Role of autophagy and its significance in cellular homeostasis

Awan, Muhammad Umer Farooq; Deng, Yulin

doi:10.1007/s00253-014-5721-8

Cited by 34 publications

(33 citation statements)

References 107 publications

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“…The protein products of Atgs are organized in five functional groups, namely: (i) the Unc-51-like kinase (Ulk):Atg13:FIP200 initiation complex (Ganley et al, 2009; Hosokawa et al, 2009); (ii) the beclin1:hVps34[phosphatidylinositol 3 (PI3) kinase]:Atg14L nucleation complex (Itakura et al, 2008); (iii) the PI3–phosphate-binding WIPI-1/2 complex (Proikas-Cezanne et al, 2004; Vergne et al, 2009); (iv) the Atg5–Atg12 conjugation complex activated by Atg7 (Mizushima et al, 1998); and (v) the Atg8 (LC3) conjugation system (Kabeya et al, 2000). These protein complexes participate at specific stages in the autophagic process: initiation, formation, elongation, and fusion (Mehrpour et al, 2010; Awan and Deng, 2014); they are also controlled by several other signaling pathways that fine tune autophagy to regulate the pace of autophagosome formation.…”

Section: Autophagy and Its Role In Skeletal Muscle Homeostasismentioning

confidence: 99%

Skeletal Muscle Homeostasis in Duchenne Muscular Dystrophy: Modulating Autophagy as a Promising Therapeutic Strategy

Palma

Perrotta

Pellegrino

et al. 2014

Front. Aging Neurosci.

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Muscular dystrophies are a group of genetic and heterogeneous neuromuscular disorders characterized by the primary wasting of skeletal muscle. In Duchenne muscular dystrophy (DMD), the most severe form of these diseases, the mutations in the dystrophin gene lead to muscle weakness and wasting, exhaustion of muscular regenerative capacity, and chronic local inflammation leading to substitution of myofibers by connective and adipose tissue. DMD patients suffer from continuous and progressive skeletal muscle damage followed by complete paralysis and death, usually by respiratory and/or cardiac failure. No cure is yet available, but several therapeutic approaches aiming at reversing the ongoing degeneration have been investigated in preclinical and clinical settings. Autophagy is an important proteolytic system of the cell and has a crucial role in the removal of proteins, aggregates, and organelles. Autophagy is constantly active in skeletal muscle and its role in tissue homeostasis is complex: at high levels, it can be detrimental and contribute to muscle wasting; at low levels, it can cause weakness and muscle degeneration, due to the unchecked accumulation of damaged proteins and organelles. The causal relationship between DMD pathogenesis and dysfunctional autophagy has been recently investigated. At molecular level, the Akt axis is one of the key dysregulated pathways, although the molecular events are not completely understood. The aim of this review is to describe and discuss the clinical relevance of the recent advances dissecting autophagy and its signaling pathway in DMD. The picture might pave the way for the development of interventions that are able to boost muscle growth and/or prevent muscle wasting.

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Section: Autophagy and Its Role In Skeletal Muscle Homeostasismentioning

confidence: 99%

Skeletal Muscle Homeostasis in Duchenne Muscular Dystrophy: Modulating Autophagy as a Promising Therapeutic Strategy

Palma

Perrotta

Pellegrino

et al. 2014

Front. Aging Neurosci.

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“…Autophagy is regarded as a cellular self-digestion process in response to a wide range of deleterious stimuli, through which cytoplasmic materials or organelles integrate into lysosomes for further degradation (47). Previous studies have reported that, autophagy serves a crucial role in the development, differentiation, survival and homeostasis of cells (48)(49)(50)(51). During organ I/R injury, autophagy may help cells respond to injury.…”

Section: Discussionmentioning

confidence: 99%

BM‑MSCs protect against liver ischemia/reperfusion injury via HO‑1 mediated autophagy

Wang

Zhou

et al. 2018

Mol Med Report

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Ischemia/reperfusion (I/R) injury is considered to be a contributing factor in liver injury following major hepatic resection or liver transplantation. Bone marrow mesenchymal stem cells (BM‑MSCs) have the potential to protect against liver I/R injury; however, the precise mechanisms have not been completely elucidated. Autophagy serves an important role in protecting against various injuries, including I/R injury. The present study aimed to determine the role of autophagy and its potential regulatory mechanism in BM‑MSC‑mediated protection against liver I/R injury in rats. The results demonstrated that BM‑MSCs mitigated I/R injury and enhanced autophagy in vivo. In addition, inhibition of autophagy by 3‑methyladenine reversed the positive effects of BM‑MSCs. Furthermore, heme oxygenase‑1 (HO‑1) expression was promoted by BM‑MSCs. Using zinc protoporphyrin IX to inhibit HO‑1 demonstrated that HO‑1 was important for the promotion of autophagy. In conclusion, the present study revealed that BM‑MSCs protected against liver I/R injury via the promotion of HO‑1‑mediated autophagy.

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“…Autophagosome maturity occurs through fusion with the lysosome, which contains lysosomal acid proteases that degrade the engulfed materials( Figure 3; Awan & Deng, 2014;Glick et al, 2010;Jiang et al, 2014;Mizushima, 2007;Mizushima, Yoshimori, & Ohsumi, 2011).…”

Section: Autophagymentioning

confidence: 99%