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<title cf:type="text"><![CDATA[Progress in Biochemistry and Biophysics -->Special Topic: Sports and Health]]></title>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[<b>Rapid Communications:<.b> Exercise Alleviates ER Reductive Stress and Promotes Healthy Aging]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20220057]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<b>Objective</b> Exercise has been approved as an effective anti-aging approach. However, how exercise affects the organelle-specific redox status of the endoplasmic reticulum (ER) and whether it contributes to ER function and healthy aging are still unknown.<b>Methods</b> We constructed an ER-specific reductive stress <i>C. elegans </i>model that overexpresses<i> ctl-1</i>, a homolog of the mammalian catalase gene, to research the effect of ER reductive stress on aging at the organismal level. We then used the Hyperion<sub>ER</sub> probe which responds well to hydrogen peroxide to evaluate the redox status in the ER of body wall muscle during swimming and during aging.<b>Results</b> Our results show that H<sub>2</sub>O<sub>2</sub> in the ER was markedly reduced during aging and the number of body bending, the life span and the stress response ability in <i>Pnfya-1</i>::<i>ctl-1<sub>ER</sub></i>::<i>mCherry</i> <i>C. elegans </i>was markedly decreased compared with that in <i>Pnfya-1</i>::<i>ctl-1-M<sub>ER</sub></i>::<i>mCherry</i>, indicating that ER reductive stress occurs during the aging process and ER reductive stress promotes aging at the organismal level. Both short-term and long-term exercise can increase the oxidative power of the ER in <i>C. elegans</i>, and exercise alleviates the age-related ER reductive stress and promotes healthy aging.<b>Conclusion</b> Our results demonstrate the effect of exercise on ER redox status at the organelle level for the first time and uncover a new mechanism for exercise in delaying aging at the organismal level from the redox point of view, suggesting that maintaining the oxidation power of the ER may be a valuable geroprotective strategy.]]></description>
<pubDate>2022/3/21 0:00:00</pubDate>
<category><![CDATA[Special Topic: Sports and Health]]></category>
<author><![CDATA[WANG Yuan-Yuan,QIAO Xin-Hua,SHI Chang,YE Ao-Jun,GUO Miao-Miao,ZHAO Yu-Zheng and CHEN Chang]]></author>
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<atom:name>WANG Yuan-Yuan,QIAO Xin-Hua,SHI Chang,YE Ao-Jun,GUO Miao-Miao,ZHAO Yu-Zheng and CHEN Chang</atom:name>
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<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20220057]]></guid><cfi:id>7</cfi:id><cfi:read>true</cfi:read></item>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[<b>Review: </b>Research Progress of Exercise and Protein Acylation]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20220079]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Protein acylation is a type of protein post-translational modification. Novel acylations except for acetylation, have been expanded successively in recent years. Histone acylation can directly modulate the packaging of chromatin either by altering the net charge of histone molecules or by altering inter-nucleosomal interactions, thereby promoting the regulation of transcription in the nucleus and the gene expression; besides, acylation can regulate the structure and function of non-histone protein, which changes in protein interactions between its binding partners, widely participating in a variety of cellular and molecular biological regulation. Exercise is one of the most critical factors that affect protein acylation, it not only enhances histone acylation level and involves in the regulation of gene expression, but also maintains tissue and cell metabolic homeostasis by regulating the histone acetyl transferases/histone deacetylases. Exercise modulates protein acylation through two pathways. On one hand, exercise regulates substance metabolism to change the level of metabolite in the human body, which provides abundant acyl-donors for acylation, such as acetyl-coenzyme A, succinyl-coenzyme A and lactoyl-coenzyme A. The acyl-coenzyme A comes from the intermediate products of glucose, fatty acids and amino acids metabolism in the body. Exercise-induced enhanced metabolism, increased tricarboxylic acid cycle rate, changes in energy content and enzyme activity all affect the concentration of acyl-CoA, thereby affecting the overall acylation level in a more three-dimensional and multi-dimensional manner. On the other hand, dramatic redox reactions and changes in kinase activity during exercise can also change the expression and activity of deacetylases such as the sirtuins family, regulating the balance of acylation/deacylation. Redox reactions in the intracellular surge during exercise cause an increase in the NAD<sup>+</sup>/NADH ratio, and can clearly activate sirtuins. In addition, altered levels of active factors and kinases can also promote gene and protein expression of enzymes and regulate deacylation. Briefly, the regulation of exercise on protein acylation is a new mechanism for exercise that improves metabolism, promotes health and prevents chronic diseases, relevant research work is still in its infancy and deserves special focus.<label></label><fig orientation="portrait" position="float" fig-type="abstract-image" id="F1"></fig>]]></description>
<pubDate>2022/3/21 0:00:00</pubDate>
<category><![CDATA[Special Topic: Sports and Health]]></category>
<author><![CDATA[HUANG Wen-Hua,ZHANG Jing-Bo,CHEN Xue-Fei and ZHANG Jing]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>HUANG Wen-Hua,ZHANG Jing-Bo,CHEN Xue-Fei and ZHANG Jing</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20220079]]></guid><cfi:id>6</cfi:id><cfi:read>true</cfi:read></item>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[<b>Review: </b>Biological Clock <i>Bmal1</i> Gene and Chronic Metabolic Diseases and Exercise Intervention Research Progress]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20210304]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Brain and muscle arnt-like protein 1 (<i>Bmal1</i>) is the core gene of biological clock, which belongs to the transcription factor family of bHLH-PAS (basic helix-loop-helix-per-arnt-sim) domain. It can regulate the circadian rhythm through its own expression and the transcription-translation feedback regulation of the biological clock, which plays an important role in the life activities of organism. The disorder of biological clock induces a series of chronic metabolic diseases, such as cardiovascular diseases, hepatopathy and neurodegenerative diseases, usually accompanied by abnormal expression of <i>Bmal1</i>. Exercise may up-regulate <i>Bmal1</i> expression in peripheral tissues and organs to improve chronic metabolic diseases. Different exercise loads and types of exercise, such as aerobic exercise, resistance exercise, will lead to the differential expression of <i>Bmal1</i>. There are many potential mechanisms of <i>Bmal1</i> in improving chronic metabolic diseases by exercise intervention, such as reducing inflammation and oxidative stress, regulating autophagy, maintaining mitochondrial quality and function, interacting with exerkines and microRNA. This article reviews the physiological function of <i>Bmal1</i> in multiple tissues and organs and the relationship between corresponding chronic metabolic diseases, discussing the influence of exercise intervention on <i>Bmal1</i> expression deeply and putting forward the potential mechanism of <i>Bmal1</i> in improving chronic metabolic diseases by exercise, in order to provide a new perspective for exercise as a non-drug treatment to prevent and treat chronic metabolic diseases.]]></description>
<pubDate>2022/3/21 0:00:00</pubDate>
<category><![CDATA[Special Topic: Sports and Health]]></category>
<author><![CDATA[DI Ling-Yun and TIAN Zhen-Jun]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>DI Ling-Yun and TIAN Zhen-Jun</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20210304]]></guid><cfi:id>5</cfi:id><cfi:read>true</cfi:read></item>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[<b>Review: </b>Exercise Induced Hypoalgesia: Spinal, Subcortical, and Cortical Mechanisms]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20210291]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Exercise with adequate intensity and duration or specialized exercise therapy have been widely proven to be effective in enhancing pain thresholds or increasing pain tolerance in healthy subjects or chronic pain patients. Exercise induced hypoalgesia (EIH) may involve various central structures in the endogenous pain modulation; motor stimulation with different types can activate either spinal cord induced local inhibition or supraspinal structures induced descending pain inhibition influencing the nociception at the spinal cord level. At the spinal level, continued exercise can down-regulate the expression of IL-1β, IL-6 and TNF-α, while the transient hypoalgesia effect of voluntary movement could be elicited by gate control of the dorsal horn; at supraspinal and subcortical levels, endogenous opioids, cannabinoids, and 5-HT-related descending inhibition of PAG and RVM can be modulated by exercise with different intensity, while the nociceptive discrimination of the thalamus and cognitive processing of the basal amygdala might also be affected by the somatosensory input of exercise, respectively; at cortical level, M1 can be activated by voluntary movement, rTMS or tDCS showed a significant antinociceptive effect in patients with chronic pain, while the DLPFC, MOPFC and insula associated with exercise have also been proven to participate in the EIH effect. In pathological pain state, the EIH is affected with the limited activity of motor cortex and the impaired function of descending pain inhibition, while the active treatment with exercise at non-affected body parts can still partially reverse the pain sensitization and induce the EIH effect. The investigation of EIH effect at spinal, subcortical and cortical levels will assist one to better understand EIH mechanisms, and help to provide the prevention of chronic pain <i>via</i> non-pharmacological exercise therapy.]]></description>
<pubDate>2022/3/21 0:00:00</pubDate>
<category><![CDATA[Special Topic: Sports and Health]]></category>
<author><![CDATA[XU Zi-Han and YOU Hao-Jun]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>XU Zi-Han and YOU Hao-Jun</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20210291]]></guid><cfi:id>4</cfi:id><cfi:read>true</cfi:read></item>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[<b>Review: </b>Research Progress on Prevention and Treatment of Sarcopenia by Exercise Induced Exosomes]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20210085]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Sarcopenia is an aging syndrome characterized by progressive decline of skeletal muscle mass and strength. It is a great significance to explore its pathogenesis for the treatment and prevention of sarcopenia. Studies have shown that exosomes are closely related to sarcopenia, and may be a useful means of weakening/preventing sarcopenia, but its underlying mechanism remains unclear. Recent studies have shown that exosomes are rich in exerkines/cytokines, which not only participate in the “cross talk” between cells and tissues, but also mediate many pathophysiological processes including the proliferation and differentiation of skeletal muscle cells. Moreover, exercise can effectively improve sarcopenia by promoting the release of exosomes and regulating the expression of miRNAs and/or proteins carried by exosomes. In this paper, we summarized the exosomes and their biological characteristics, as well as the relationship between exosomes and sarcopenia. Firstly, exosomes themselves or the carried mRNA are involved in the aging, promoting the secretion of inflammatory factors and weakening the muscle protein breakdown (MPB) pathway, indicating the exosomes is important to improve the pathology of sarcopenia. There is a strategy for delaying MPB in sarcopenia by increasing the concentration and number of exosomes in skeletal muscle cells. Secondly, exosomes are closely associated with exercise. Both acute and long-term endurance exercise may promote the release of exosomes and induce a “qualitative” change in exosomes. Moreover, we also analyzed the influence of exercise on exosomes and its underlying mechanism. The underlying mechanism is that exercise would improve skeletal muscle homeostasis through activation of exosomes/exosomes-derived miRNAs or mediate protein degradation through activation of the PI3K/PKB/mTOR pathway, ultimately weakening sarcopenia.]]></description>
<pubDate>2022/3/21 0:00:00</pubDate>
<category><![CDATA[Special Topic: Sports and Health]]></category>
<author><![CDATA[KE Zhi-Fei,SHANG Hua-Yu,LEI Bin-Kai,CAO Chun-Xia,WANG Zhen,WANG Rui-Yuan and LI Jun-Ping]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>KE Zhi-Fei,SHANG Hua-Yu,LEI Bin-Kai,CAO Chun-Xia,WANG Zhen,WANG Rui-Yuan and LI Jun-Ping</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20210085]]></guid><cfi:id>3</cfi:id><cfi:read>true</cfi:read></item>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[<b>Review: </b>The Function of ESCRT Complex in Plasma Membrane Repair]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20210269]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Plasma membrane disruptions have been documented under physiological conditions in lots of mechanically active tissues, such as in skeletal muscle, the stratified epithelium that covers our body, the endothelia that line our blood vessels, the epithelial barrier of our gastrointestinal tract. Timely and effective plasma membrane repair (PMR) mechanisms have evolved to rapidly reseal a membrane breach to ensure cell survival. Otherwise, these membrane disruption events initiate a “death cascade”. PMR is coordinated by many “tinkerers”, which have a clear division of labor and show certain timing characteristics. The endosomal sorting complexes required for transport (ESCRT) is the “tinkerer” found recently who plays a key role in the repair of plasma membrane disruptions. It is composed of ESCRT-0, ESCRT-I, ESCRT-II, ESCRT-III, VPS4-VTA1 and ALIX, which take part in the budding and the formation of multivesicular body (MVB). This paper reviews two repair methods mediated by ESCRT system with budding and the formation of MVB. The function of ESCRT complex in plasma membrane repair can improve membrane disruptions, which is able to be used as an effective prevention and treatment strategy for cancer, Alzheimer’s disease, muscle injury and muscular dystrophy.]]></description>
<pubDate>2022/3/21 0:00:00</pubDate>
<category><![CDATA[Special Topic: Sports and Health]]></category>
<author><![CDATA[ZHAO Sha-Sha,SHI Li-Jun and WU Ying]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>ZHAO Sha-Sha,SHI Li-Jun and WU Ying</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20210269]]></guid><cfi:id>2</cfi:id><cfi:read>true</cfi:read></item>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[<b>Review: </b>Role of GPCRs in The Effect of Exercise on Bone Metabolism]]></title>
<link><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20220024]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[The bone formation metabolism dominated by osteoblasts (OB) has been restrained and the bone resorption metabolism dominated by osteoclasts (OC) is abnormally elevated, leading to bone metabolism disorders. As the key seven-transmembrane proteins that sense external signal stimuli in OBs, chondrocytes and OCs, G protein-coupled receptors (GPCRs) have been widely recognized by bone in their key regulatory roles in the differentiation and function of OBs, chondrocytes and OCs. Thus, those research results have got more attention in metabolism field. Loss of GPCRs function or abnormal increase in the homeostasis of the osteocyte homeostasis leads to the differentiation and dysfunction of OB, chondrocytes and OC, which results in bone loss and degeneration of the microstructure of bone tissue. Studies have shown that exercise is an important way to improve bone metabolism disorders by promoting bone formation and inhibiting bone resorption. The analysis found that the molecular regulation mechanism of this process is related to the key signaling pathways (cAMP/PKA/Atf4, JNK/AP-1, ERK1/2, <i>etc</i>.) and cytokines (T-PINP, Nkx3.2, Sox9 and Cleaved-caspase-3, <i>etc</i>.) are closely related to the differentiation and function of OB, chondrocytes and OC. Except from the confirmed GPR48, this review tested out the molecular mechanism of GPCRs regulating bone formation and bone resorption and their role in the effect of exercise on bone metabolism. The mechanism of other GPCRs in the improvement of bone metabolism by exercise has yet to be revealed on what kind of exercise mode and intensity can effectively regulate GPCR and improve bone metabolism and so on. The results help to screen out sensitive GPCRs on membranes as “effectors” for drug development of bone metabolic diseases and “star proteins” for mechanical stimulation in exercise intervention and provide more targets or perspectives for the research and prevention of osteoporosis.]]></description>
<pubDate>2022/3/21 0:00:00</pubDate>
<category><![CDATA[Special Topic: Sports and Health]]></category>
<author><![CDATA[CHEN Xiang-He,LIU Bo,LU Peng-Cheng,QIU Xiao,ZHOU Xiang-Xiang and ZENG Xin-Yu]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>CHEN Xiang-He,LIU Bo,LU Peng-Cheng,QIU Xiao,ZHOU Xiang-Xiang and ZENG Xin-Yu</atom:name>
</atom:author>
<guid><![CDATA[http://www.pibb.ac.cn/pibben/article/abstract/20220024]]></guid><cfi:id>1</cfi:id><cfi:read>true</cfi:read></item>
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