Autophagy and inflammation in chronic respiratory disease

Racanelli, Alexandra C.; Kikkers, Sarah Ann; Choi, Augustine M.K.; Cloonan, Suzanne M.

doi:10.1080/15548627.2017.1389823

Cited by 392 publications

(309 citation statements)

References 113 publications

(175 reference statements)

Supporting

Mentioning

297

Contrasting

Unclassified

Order By: Relevance

“…Studies have confirmed that the inhibition of adipose-specific autophagy leads to the increased number of adipocytes with features of brown adipocytes. This facilitated fatty acid oxidation and increased insulin sensitivity both in vitro and in vivo [26]. We speculate that Mark4, autophagy, and browning of white adipose tissue have certain linkages, whether Mark4 can influence autophagy has not been reported.…”

Section: Discussionmentioning

confidence: 87%

Mark4 Inhibited the Browning of White Adipose Tissue by Promoting Adipocytes Autophagy in Mice

Yang

Cai

Pan

et al. 2020

IJMS

View full text Add to dashboard Cite

Autophagy can remove excess or dysfunctional proteins and organelles to maintain cellular homeostasis. Browning of white adipose tissue increases the energy expenditure. Microtubules affinity regulated kinase 4 (Mark4) can regulate a variety of physiological processes. According to previous studies, we speculated that Mark4-autophagy-browning of white adipose tissue had certain linkages. Here, we established two autophagy models through serum starvation and rapamycin treatment and detected that the overexpression of Mark4 increased the expression of autophagy-related factors Beclin1, ATG7, and significantly decreased the autophagy substrate P62. Further tests showed that the overexpression of Mark4 promoted the conversion of autophagy marker protein LC3A to LC3B-II by activating the AMP-activated protein kinase (AMPK) pathway and inhibition of the AKT/mTOR signaling. Moreover, Mark4 decreased the expression of thermogenesis genes via promoting autophagy. These results indicated that Mark4 inhibited the browning of white adipose tissue via promoting autophagy. AMPK signaling pathway. By adding compound C, the phosphorylation of AMPK and the formation of LC3B-II were reduced while the level of autophagy substrate p62 was increased ( Figure 4A,B). The results of AKT pathway examination was opposite. The overexpression of Mark4 significantly inhibited the phosphorylation of AKT and mTOR, accompanied by an increase in LC3B-II and a decrease in P62. After treating with the AKT inhibitor MK2206, the phosphorylation levels of AKT, mTOR, and the protein level of P62 were significantly reduced. The LC3B-II expression was increased ( Figure 4C,D). These results indicated that Mark4 could regulate serum starvation-induced autophagy via the AMPK/AKT signal pathway.

show abstract

Section: Discussionmentioning

confidence: 87%

Mark4 Inhibited the Browning of White Adipose Tissue by Promoting Adipocytes Autophagy in Mice

Yang

Cai

Pan

et al. 2020

IJMS

View full text Add to dashboard Cite

show abstract

“…Evidence suggests emphysema is caused by accelerated ageing of lung tissues and is associated with flawed endogenous antiageing (sirtuins) and autophagy mechanisms [106][107][108]. This process leads to eventual telomere shortening, cellular senescence, and the development of COPD [109,110]. Oxidative stress is another key driver of COPD pathogenesis.…”

Section: Molecular Mechanisms Of Disease Progressionmentioning

confidence: 99%

Animal Models Reflecting Chronic Obstructive Pulmonary Disease and Related Respiratory Disorders: Translating Pre-Clinical Data into Clinical Relevance

Tanner

Single

2019

J Innate Immun

View full text Add to dashboard Cite

Chronic obstructive pulmonary disease (COPD) affects the lives of an ever-growing number of people worldwide. The lack of understanding surrounding the pathophysiology of the disease and its progression has led to COPD becoming the third leading cause of death worldwide. COPD is incurable, with current treatments only addressing associated symptoms and sometimes slowing its progression, thus highlighting the need to develop novel treatments. However, this has been limited by the lack of experimental standardization within the respiratory disease research area. A lack of coherent animal models that accurately represent all aspects of COPD clinical presentation makes the translation of promising in vitro data to human clinical trials exceptionally challenging. Here, we review current knowledge within the COPD research field, with a focus on current COPD animal models. Moreover, we include a set of advantages and disadvantages for the selection of pre-clinical models for the identification of novel COPD treatments.

show abstract

“…Autophagy is a well-organized homeostatic cellular process through which diverse cytoplasmic cargos are captured and destroyed to replenish energy sources and amino acids during metabolic stress. 1,2 Autophagy process comprises three steps: the first step is when autophagy-related gene (ATG) drives the cupshaped isolation membrane to decompose into phagophores with omegasome, an autophagic intermediate formed by the endoplasmic reticulum, in the cytosol. Next, the phagophores sequester the cell contents used for autophagy and form autophagosome with a double-membrane structure by elongation and closure.…”

mentioning

confidence: 99%

MicroRNAs play an essential role in autophagy regulation in various disease phenotypes

et al. 2019

View full text Add to dashboard Cite

Autophagy is a highly conserved catabolic process and fundamental biological process in eukaryotic cells. It recycles intracellular components to provide nutrients during starvation and maintains quality control of organelles and proteins. In addition, autophagy is a well‐organized homeostatic cellular process that is responsible for the removal of damaged organelles and intracellular pathogens. Moreover, it also modulates the innate and adaptive immune systems. Micro ribonucleic acids (microRNAs) are a mature class of post‐transcriptional modulators that are widely expressed in tissues and organs. And, it can suppress gene expression by targeting messenger RNAs for translational repression or, at a lesser extent, degradation. Research indicates that microRNAs regulate autophagy through different pathways, playing an essential role in the treatment of various diseases. It is an important regulator of fundamental cellular processes such as proliferation, autophagy, and cell apoptosis. In this review article, we first review the current knowledge of autophagy and the function of microRNAs. Then, we summarize the mechanism of autophagy and the signaling pathways related to autophagy by citing at least the main proteins involved in the different phases of the process. Second, we introduce other members of RNA and report some examples in various pathologies. Finally, we review the current literature regarding microRNA‐based therapies for cancer, atherosclerosis, cardiac disease, tuberculosis, and viral diseases. MicroRNAs can cause autophagy upregulation or downregulation by targeting genes or affecting autophagy‐related signaling pathways. Therefore, the microRNAs have a huge potential in autophagy regulation, and it is the function as diagnostic and prognostic markers.

show abstract

Autophagy and inflammation in chronic respiratory disease

Cited by 392 publications

References 113 publications

Mark4 Inhibited the Browning of White Adipose Tissue by Promoting Adipocytes Autophagy in Mice

Mark4 Inhibited the Browning of White Adipose Tissue by Promoting Adipocytes Autophagy in Mice

Animal Models Reflecting Chronic Obstructive Pulmonary Disease and Related Respiratory Disorders: Translating Pre-Clinical Data into Clinical Relevance

MicroRNAs play an essential role in autophagy regulation in various disease phenotypes

Contact Info

Product

Resources

About