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BMB Reports update

Biochemistry and Molecular Biology Reports

  • : 생화학분자생물학회(구 한국생화학분자생물학회)
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  • : Korean Biochemical Journal(~1994)→Journal of Biochemistry and Molecular Biology(1995~)→Biochemistry and Molecurar Biology Reports(2008~)

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수록범위 : 1권1호(1968)~52권1호(2019) |수록논문 수 : 4,276
BMB Reports
52권1호(2019년) 수록논문
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KCI등재 SCI SCOPUS

1Cellular senescence, aging, and age-related disease: Special issue of BMB Reports in 2019

저자 : Jae-seon Lee

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 52권 1호 발행 연도 : 2019 페이지 : pp. 1-2 (2 pages)

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KCI등재 SCI SCOPUS

2Juxtacrine regulation of cellular senescence

저자 : Masashi Narita

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 52권 1호 발행 연도 : 2019 페이지 : pp. 3-4 (2 pages)

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Cellular senescence is defined as a state of stable cell cycle exit in response to various stimuli, which include both cytotoxic stress and physiological cues. In addition to the core non-proliferative aspect, senescence is associated with diverse functionalities, which contribute to the role of senescence in a wide range of pathological and physiological processes. Such functionality is often mediated by the capability of senescent cells to communicate with their surroundings. Emerging evidence suggests that senescence is not a single entity, but a dynamic and heterogeneous collective phenotype. Understanding the diverse nature of senescence should provide insights into the complexity of tissue homeostasis and its disruption, such as in aging and tumorigenesis. [BMB Reports: Perspective 2019; 52(1): 3-4]

KCI등재 SCI SCOPUS

3Metabolic features and regulation in cell senescence

저자 : So Mee Kwon , Sun Mi Hong , Young-kyoung Lee , Seongki Min , Gyesoon Yoon

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 52권 1호 발행 연도 : 2019 페이지 : pp. 5-12 (8 pages)

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Organismal aging is accompanied by a host of progressive metabolic alterations and an accumulation of senescent cells, along with functional decline and the appearance of multiple diseases. This implies that the metabolic features of cell senescence may contribute to the organism's metabolic changes and be closely linked to age-associated diseases, especially metabolic syndromes. However, there is no clear understanding of senescent metabolic characteristics. Here, we review key metabolic features and regulators of cellular senescence, focusing on mitochondrial dysfunction and anabolic deregulation, and their link to other senescence phenotypes and aging. We further discuss the mechanistic involvement of the metabolic regulators mTOR, AMPK, and GSK3, proposing them as key metabolic switches for modulating senescence. [BMB Reports 2019; 52(1): 5-12]

KCI등재 SCI SCOPUS

4Mitochondria: multifaceted regulators of aging

저자 : Jyung Mean Son , Changhan Lee

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 52권 1호 발행 연도 : 2019 페이지 : pp. 13-23 (11 pages)

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Aging is accompanied by a time-dependent progressive deterioration of multiple factors of the cellular system. The past several decades have witnessed major leaps in our understanding of the biological mechanisms of aging using dietary, genetic, pharmacological, and physical interventions. Metabolic processes, including nutrient sensing pathways and mitochondrial function, have emerged as prominent regulators of aging. Mitochondria have been considered to play a key role largely due to their production of reactive oxygen species (ROS), resulting in DNA damage that accumulates over time and ultimately causes cellular failure. This theory, known as the mitochondrial free radical theory of aging (MFRTA), was favored by the aging field, but increasing inconsistent evidence has led to criticism and rejection of this idea. However, MFRTA should not be hastily rejected in its entirety because we now understand that ROS is not simply an undesired toxic metabolic byproduct, but also an important signaling molecule that is vital to cellular fitness. Notably, mitochondrial function, a term traditionally referred to bioenergetics and apoptosis, has since expanded considerably. It encompasses numerous other key biological processes, including the following: (i) complex metabolic processes, (ii) intracellular and endocrine signaling/communication, and (iii) immunity/inflammation. Here, we will discuss shortcomings of previous concepts regarding mitochondria in aging and their emerging roles based on recent advances. We will also discuss how the mitochondrial genome integrates with major theories on the evolution of aging. [BMB Reports 2019; 52(1): 13-23]

KCI등재 SCI SCOPUS

5Sirtuin signaling in cellular senescence and aging

저자 : Shin-hae Lee , Ji-hyeon Lee , Hye-yeon Lee , Kyung-jin Min

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 52권 1호 발행 연도 : 2019 페이지 : pp. 24-34 (11 pages)

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Sirtuin is an essential factor that delays cellular senescence and extends the organismal lifespan through the regulation of diverse cellular processes. Suppression of cellular senescence by Sirtuin is mainly mediated through delaying the age-related telomere attrition, sustaining genome integrity and promotion of DNA damage repair. In addition, Sirtuin modulates the organismal lifespan by interacting with several lifespan regulating signaling pathways including insulin/IGF-1 signaling pathway, AMP-activated protein kinase, and forkhead box O. Although still controversial, it is suggested that the prolongevity effect of Sirtuin is dependent with the level of and with the tissue expression of Sirtuin. Since Sirtuin is also believed to mediate the prolongevity effect of calorie restriction, activators of Sirtuin have attracted the attention of researchers to develop therapeutics for age-related diseases. Resveratrol, a phytochemical rich in the skin of red grapes and wine, has been actively investigated to activate Sirtuin activity with consequent beneficial effects on aging. This article reviews the evidences and controversies regarding the roles of Sirtuin on cellular senescence and lifespan extension, and summarizes the activators of Sirtuin including Sirtuin-activating compounds and compounds that increase the cellular level of nicotinamide dinucleotide. [BMB Reports 2019; 52(1): 24-34]

KCI등재 SCI SCOPUS

6Cellular senescence: a promising strategy for cancer therapy

저자 : Seongju Lee , Jae-seon Lee

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 52권 1호 발행 연도 : 2019 페이지 : pp. 35-41 (7 pages)

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Cellular senescence, a permanent state of cell cycle arrest, is believed to have originally evolved to limit the proliferation of old or damaged cells. However, it has been recently shown that cellular senescence is a physiological and pathological program contributing to embryogenesis, immune response, and wound repair, as well as aging and age-related diseases. Unlike replicative senescence associated with telomere attrition, premature senescence rapidly occurs in response to various intrinsic and extrinsic insults. Thus, cellular senescence has also been considered suppressive mechanism of tumorigenesis. Current studies have revealed that therapy-induced senescence (TIS), a type of senescence caused by traditional cancer therapy, could play a critical role in cancer treatment. In this review, we outline the key features and the molecular pathways of cellular senescence. Better understanding of cellular senescence will provide insights into the development of powerful strategies to control cellular senescence for therapeutic benefit. Lastly, we discuss existing strategies for the induction of cancer cell senescence to improve efficacy of anticancer therapy. [BMB Reports 2019; 52(1): 35-41]

KCI등재 SCI SCOPUS

7Cellular senescence in cancer

저자 : Young Hwa Kim , Tae Jun Park

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 52권 1호 발행 연도 : 2019 페이지 : pp. 42-46 (5 pages)

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Cellular senescence, a process of cell proliferation arrest in response to various stressors, has been considered to be important factor in age-related disease. Identification of senescent cells in tissues is limited and the role of senescent cells is poorly understood. Recently however, several studies showed the characterization of senescent cells in various pathologic conditions and the role of senescent cells in disease progression is becoming important. Senescent cells are growth-arrested cells, however, the senescence associated secretory phenotype (SASP) of senescent cells could modify the tissues' microenvironment. Here, we discuss the progress and understanding of the role of senescent cells in tissues of pathologic conditions and discuss the development of new therapeutic paradigms, such as senescent cells-targeted therapy. [BMB Reports 2019; 52(1): 42-46]

KCI등재 SCI SCOPUS

8Senotherapeutics: emerging strategy for healthy aging and age-related disease

저자 : Eok-cheon Kim , Jae-ryong Kim

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 52권 1호 발행 연도 : 2019 페이지 : pp. 47-55 (9 pages)

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Cellular senescence (CS) is one of hallmarks of aging and accumulation of senescent cells (SCs) with age contributes to tissue or organismal aging, as well as the pathophysiologies of diverse age-related diseases (ARDs). Genetic ablation of SCs in tissues lengthened health span and reduced the risk of age-related pathologies in a mouse model, suggesting a direct link between SCs, longevity, and ARDs. Therefore, senotherapeutics, medicines targeting SCs, might be an emerging strategy for the extension of health span, and prevention or treatment of ARDs. Senotherapeutics are classified as senolytics which kills SCs selectively; senomorphics which modulate functions and morphology of SCs to those of young cells, or delays the progression of young cells to SCs in tissues; and immune-system mediators of the clearance of SCs. Some senolytics and senomorphics have been proven to markedly prevent or treat ARDs in animal models. This review will present the current status of the development of senotherapeutics, in relation to aging itself and ARDs. Finally, future directions and opportunities for senotherapeutics use will discussed. This knowledge will provide information that can be used to develop novel senotherapeutics for health span and ARDs. [BMB Reports 2019; 52(1): 47-55]

KCI등재 SCI SCOPUS

9Modulation of senoinflammation by calorie restriction based on biochemical and Omics big data analysis

저자 : Eunjin Bang , Bonggi Lee , Sang-gyun Noh , Dae Hyun Kim , Hee Jin Jung , Sugyeong Ha , Byung Pal Yu , Hae Young Chung

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 52권 1호 발행 연도 : 2019 페이지 : pp. 56-63 (8 pages)

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Aging is a complex and progressive process characterized by physiological and functional decline with time that increases susceptibility to diseases. Aged-related functional change is accompanied by a low-grade, unresolved chronic inflammation as a major underlying mechanism. In order to explain aging in the context of chronic inflammation, a new integrative concept on age-related chronic inflammation is necessary that encompasses much broader and wider characteristics of cells, tissues, organs, systems, and interactions between immune and non-immune cells, metabolic and non-metabolic organs. We have previously proposed a novel concept of senescent (seno)-inflammation and provided its frameworks. This review summarizes senoinflammation concept and additionally elaborates modulation of senoinflammation by calorie restriction (CR). Based on aging and CR studies and systems-biological analysis of Omics big data, we observed that senescence associated secretory phenotype (SASP) primarily composed of cytokines and chemokines was notably upregulated during aging whereas CR suppressed them. This result further strengthens the novel concept of senoinflammation in aging process. Collectively, such evidence of senoinflammation and modulatory role of CR provide insights into aging mechanism and potential interventions, thereby promoting healthy longevity. [BMB Reports 2019; 52(1): 56-63]

KCI등재 SCI SCOPUS

10Sarcopenia targeting with autophagy mechanism by exercise

저자 : Sung Sup Park , Young-kyo Seo , Ki-sun Kwon

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 52권 1호 발행 연도 : 2019 페이지 : pp. 64-69 (6 pages)

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The loss of skeletal muscle, called sarcopenia, is an inevitable event during the aging process, and significantly impacts quality of life. Autophagy is known to reduce muscle atrophy caused by dysfunctional organelles, even though the molecular mechanism remains unclear. Here, we have discuss the current understanding of exercise-induced autophagy activation in skeletal muscle regeneration and remodeling, leading to sarcopenia intervention. With aging, dysregulation of autophagy flux inhibits lysosomal storage processes involved in muscle biogenesis. AMPK-ULK1 and the FoxO/PGC-1α signaling pathways play a critical role in the induction of autophagy machinery in skeletal muscle, thus these pathways could be targets for therapeutics development. Autophagy has been also shown to be a critical regulator of stem cell fate, which determines satellite cell differentiation into muscle fiber, thereby increasing muscle mass. This review aims to provide a comprehensive understanding of the physiological role of autophagy in skeletal muscle aging and sarcopenia. [BMB Reports 2019; 52(1): 64-69]

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