{"title":"Ultrasound contrast agents from microbubbles to biogenic gas vesicles.","authors":"Wenlong Zeng, Xiuli Yue, Zhifei Dai","doi":"10.1515/mr-2022-0020","DOIUrl":"10.1515/mr-2022-0020","url":null,"abstract":"<p><p>Microbubbles have been the earliest and most widely used ultrasound contrast agents by virtue of their unique features: such as non-toxicity, intravenous injectability, ability to cross the pulmonary capillary bed, and significant enhancement of echo signals for the duration of the examination, resulting in essential preclinical and clinical applications. The use of microbubbles functionalized with targeting ligands to bind to specific targets in the bloodstream has further enabled ultrasound molecular imaging. Nevertheless, it is very challenging to utilize targeted microbubbles for molecular imaging of extravascular targets due to their size. A series of acoustic nanomaterials have been developed for breaking free from this constraint. Especially, biogenic gas vesicles, gas-filled protein nanostructures from microorganisms, were engineered as the first biomolecular ultrasound contrast agents, opening the door for more direct visualization of cellular and molecular function by ultrasound imaging. The ordered protein shell structure and unique gas filling mechanism of biogenic gas vesicles endow them with excellent stability and attractive acoustic responses. What's more, their genetic encodability enables them to act as acoustic reporter genes. This article reviews the upgrading progresses of ultrasound contrast agents from microbubbles to biogenic gas vesicles, and the opportunities and challenges for the commercial and clinical translation of the nascent field of biomolecular ultrasound.</p>","PeriodicalId":74151,"journal":{"name":"Medical review (Berlin, Germany)","volume":"3 1","pages":"31-48"},"PeriodicalIF":0.0,"publicationDate":"2022-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/78/00/mr-3-1-mr-2022-0020.PMC10471104.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10363192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Trimethylamine-N-oxide is an important target for heart and brain diseases.","authors":"Shusi Ding, Jing Xue, Qi Zhang, Lemin Zheng","doi":"10.1515/mr-2022-0026","DOIUrl":"10.1515/mr-2022-0026","url":null,"abstract":"Trimethylamine-N-oxide (TMAO) is a metabolite produced","PeriodicalId":74151,"journal":{"name":"Medical review (Berlin, Germany)","volume":"2 4","pages":"321-323"},"PeriodicalIF":0.0,"publicationDate":"2022-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c3/cc/mr-2-4-mr-2022-0026.PMC10388736.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10311415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The polarizable and reprogrammable identity of Kupffer cells in Nonalcoholic Steatohepatitis.","authors":"Tarik Zahr, Kevin Sun, Li Qiang","doi":"10.1515/mr-2022-0023","DOIUrl":"10.1515/mr-2022-0023","url":null,"abstract":"<p><p>Kupffer cells (KCs) are the resident macrophages of the liver with similar origins to myeloid-derived macrophages. Once differentiated, KCs exhibit distinct cellular machinery capable of longevity and self-renewal, making them a crucial player in promoting effective intrahepatic communication. However, this gets compromised in disease states like Nonalcoholic Steatohepatitis (NASH), where the loss of embryo-derived KCs (EmKCs) is observed. Despite this, other KC-like and KC-derived populations start to form and contribute to a variety of roles in NASH pathogenesis, often adopting a NASH-associated molecular signature. Here we offer a brief overview of recent reports describing KC polarization and reprogramming in the liver. We describe the complexities of KC cellular identity, their proposed ability to reprogram to fibroblast-like and endothelial-like cells, and the potential implications in NASH.</p>","PeriodicalId":74151,"journal":{"name":"Medical review (Berlin, Germany)","volume":"2 4","pages":"324-327"},"PeriodicalIF":0.0,"publicationDate":"2022-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/13/c7/mr-2-4-mr-2022-0023.PMC10388795.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10311416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Crosstalk between bone and other organs.","authors":"Wanqiong Yuan, Chunli Song","doi":"10.1515/mr-2022-0018","DOIUrl":"10.1515/mr-2022-0018","url":null,"abstract":"<p><p>Bone has long been considered as a silent organ that provides a reservoir of calcium and phosphorus, traditionally. Recently, further study of bone has revealed additional functions as an endocrine organ connecting systemic organs of the whole body. Communication between bone and other organs participates in most physiological and pathological events and is responsible for the maintenance of homeostasis. Here, we present an overview of the crosstalk between bone and other organs. Furthermore, we describe the factors mediating the crosstalk and review the mechanisms in the development of potential associated diseases. These connections shed new light on the pathogenesis of systemic diseases and provide novel potential targets for the treatment of systemic diseases.</p>","PeriodicalId":74151,"journal":{"name":"Medical review (Berlin, Germany)","volume":"2 4","pages":"331-348"},"PeriodicalIF":0.0,"publicationDate":"2022-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ae/24/mr-2-4-mr-2022-0018.PMC10471111.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10311417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Proteomics research of SARS-CoV-2 and COVID-19 disease.","authors":"Nan Zhang, Siyuan Wang, Catherine C L Wong","doi":"10.1515/mr-2022-0016","DOIUrl":"10.1515/mr-2022-0016","url":null,"abstract":"<p><p>Currently, coronavirus disease 2019 (COVID-19) is still spreading in a global scale, exerting a massive health and socioeconomic crisis. Deep insights into the molecular functions of the viral proteins and the pathogenesis of this infectious disease are urgently needed. In this review, we comprehensively describe the proteome of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and summarize their protein interaction map with host cells. In the protein interaction network between the virus and the host, a total of 787 host prey proteins that appeared in at least two studies or were verified by co-immunoprecipitation experiments. Together with 29 viral proteins, a network of 1762 proximal interactions were observed. We also review the proteomics results of COVID-19 patients and proved that SARS-CoV-2 hijacked the host's translation system, post-translation modification system, and energy supply system via viral proteins, resulting in various immune disorders, multiple cardiomyopathies, and cholesterol metabolism diseases.</p>","PeriodicalId":74151,"journal":{"name":"Medical review (Berlin, Germany)","volume":"2 4","pages":"427-445"},"PeriodicalIF":0.0,"publicationDate":"2022-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/57/66/mr-2-4-mr-2022-0016.PMC10388787.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10311418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Hypothalamic GABAergic neurocircuitry in the regulation of energy homeostasis and sleep/wake control.","authors":"Hong Jiang","doi":"10.1515/mr-2022-0022","DOIUrl":"10.1515/mr-2022-0022","url":null,"abstract":"<p><p>Gamma-aminobutyric acid (GABAergic) neuron, as one of important cell types in synaptic transmission, has been widely involved in central nervous system (CNS) regulation of organismal physiologies including cognition, emotion, arousal and reward. However, upon their distribution in various brain regions, effects of GABAergic neurons in the brain are very diverse. In current report, we will present an overview of the role of GABAergic mediated inhibitory neurocircuitry in the hypothalamus, underlying mechanism of feeding and sleep homeostasis as well as the characteristics of latest transcriptome profile in order to call attention to the GABAergic system as potentially a promising pharmaceutical intervention or a deep brain stimulation target in eating and sleep disorders.</p>","PeriodicalId":74151,"journal":{"name":"Medical review (Berlin, Germany)","volume":"2 5","pages":"531-540"},"PeriodicalIF":0.0,"publicationDate":"2022-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/6e/4d/mr-2-5-mr-2022-0022.PMC10388747.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10675081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Fibroblast growth factor 21 and dietary interventions: what we know and what we need to know next.","authors":"Tianru Jin","doi":"10.1515/mr-2022-0019","DOIUrl":"10.1515/mr-2022-0019","url":null,"abstract":"<p><p>Dietary interventions include the change of dietary styles, such as fasting and dietary or nutrient restrictions; or the addition of plant-derived compounds (such as polyphenols known as curcumin, resveratrol, or anthocyanin, or other nutraceuticals) into the diet. During the past a few decades, large number of studies have demonstrated therapeutic activities of these dietary interventions on metabolic and other diseases in human subjects or various animal models. Mechanisms underlying those versatile therapeutic activities, however, remain largely unclear. Interestingly, recent studies have shown that fibroblast growth factor 21 (FGF21), a liver-derived hormone or hepatokine, mediates metabolic beneficial effects of certain dietary polyphenols as well as protein restriction. Here I have briefly summarized functions of FGF21, highlighted related dietary interventions, and presented literature discussions on role of FGF21 in mediating function of dietary polyphenol intervention and protein restriction. This is followed by presenting my perspective view, with the involvement of gut microbiota. It is anticipated that further breakthroughs in this field in the near future will facilitate conceptual merge of classical medicine and modern medicine.</p>","PeriodicalId":74151,"journal":{"name":"Medical review (Berlin, Germany)","volume":"2 5","pages":"524-530"},"PeriodicalIF":0.0,"publicationDate":"2022-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c9/49/mr-2-5-mr-2022-0019.PMC10388781.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10657921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Challenges and opportunities in nonalcoholic steatohepatitis.","authors":"Xiaobo Wang","doi":"10.1515/mr-2022-0024","DOIUrl":"10.1515/mr-2022-0024","url":null,"abstract":"<p><p>Nonalcoholic steatohepatitis (NASH) has emerged as the leading cause of chronic liver disease worldwide and is rapidly increasing in prevalence due to the obesity epidemic. There are currently no Food and Drug Administration (FDA) approved drugs to treat NASH, and therefore a critical need exists for novel therapies that can halt or reverse the progression to hepatic fibrosis, cirrhosis, and hepatocellular carcinoma. Clinical trials to date using single drugs to treat NASH have shown disappointing efficacy. Combination therapies to attack different targets underlying disease pathogenesis of NASH are being explored as a strategy currently. Novel RNA therapies are also being developed to target previously \"undruggable\" targets and are close to the maturity necessary to be viable therapeutic approaches for the treatment of NASH and fibrosis. Identifying circulating biomarkers of fibrosis could serve as a valuable, non-invasive diagnostic tool to guide clinical practice. Despite progress in translational and clinical research, one of the major reasons for the absence of effective therapeutics is our incomplete understanding of the pathophysiology that underlies the progression from steatosis to NASH and its most deadly consequence-fibrosis. Multi-omics platforms will help to drive effective precision medicine development in NASH and hepatology.</p>","PeriodicalId":74151,"journal":{"name":"Medical review (Berlin, Germany)","volume":"2 4","pages":"328-330"},"PeriodicalIF":0.0,"publicationDate":"2022-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/2c/0c/mr-2-4-mr-2022-0024.PMC10388777.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10303012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Circadian clock and temporal meal pattern.","authors":"Xin Li, Zheng Sun","doi":"10.1515/mr-2022-0021","DOIUrl":"10.1515/mr-2022-0021","url":null,"abstract":"<p><p>The central circadian clock in the brain controls the time-of-the-day variations in acute meal responses, with a low glycemic response but a high satiety/thermogenic response to meals consumed at waking compared to other time points. Consistently, studies show that consuming a significant proportion of calories, particularly carbohydrates, in breakfast is beneficial for the chronic management of obesity and its associated metabolic syndrome, compared to consuming identical meals at dinner. Conversely, breakfast skipping or/and late dinner can have unfavorable metabolic outcomes. It remains controversial how meal frequency affects metabolic health. In contrast, irregular meals, especially irregular breakfasts, show consistent adverse metabolic consequences. Time-restricted feeding (TRF), with all calories consumed within less than 12-h per day, can improve metabolism and extend lifespan. A major component of TRF in humans is caloric restriction, which contributes significantly to the beneficial effects of TRF in humans. By comparison, TRF effects in rodents can be independent of caloric restriction and show day/night phase specificity. TRF could alleviate metabolic abnormalities due to circadian disruption, but its effects appear independent of the circadian clock in rodents. Understanding neuroendocrine mechanisms underlying clock-mediated metabolic regulation will shed light on the metabolic effects of temporal meal patterns.</p>","PeriodicalId":74151,"journal":{"name":"Medical review (Berlin, Germany)","volume":"3 1","pages":"85-101"},"PeriodicalIF":0.0,"publicationDate":"2022-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/61/2d/mr-3-1-mr-2022-0021.PMC10471112.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10363190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Leptin signaling and leptin resistance.","authors":"Jiarui Liu, Futing Lai, Yujia Hou, Ruimao Zheng","doi":"10.1515/mr-2022-0017","DOIUrl":"10.1515/mr-2022-0017","url":null,"abstract":"<p><p>With the prevalence of obesity and associated comorbidities, studies aimed at revealing mechanisms that regulate energy homeostasis have gained increasing interest. In 1994, the cloning of leptin was a milestone in metabolic research. As an adipocytokine, leptin governs food intake and energy homeostasis through leptin receptors (LepR) in the brain. The failure of increased leptin levels to suppress feeding and elevate energy expenditure is referred to as leptin resistance, which encompasses complex pathophysiological processes. Within the brain, LepR-expressing neurons are distributed in hypothalamus and other brain areas, and each population of the LepR-expressing neurons may mediate particular aspects of leptin effects. In LepR-expressing neurons, the binding of leptin to LepR initiates multiple signaling cascades including janus kinase (JAK)-signal transducers and activators of transcription (STAT) phosphatidylinositol 3-kinase (PI3K)-protein kinase B (AKT), extracellular regulated protein kinase (ERK), and AMP-activated protein kinase (AMPK) signaling, etc., mediating leptin actions. These findings place leptin at the intersection of metabolic and neuroendocrine regulations, and render leptin a key target for treating obesity and associated comorbidities. This review highlights the main discoveries that shaped the field of leptin for better understanding of the mechanism governing metabolic homeostasis, and guides the development of safe and effective interventions to treat obesity and associated diseases.</p>","PeriodicalId":74151,"journal":{"name":"Medical review (Berlin, Germany)","volume":"2 4","pages":"363-384"},"PeriodicalIF":0.0,"publicationDate":"2022-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0e/cc/mr-2-4-mr-2022-0017.PMC10388810.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10311412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}