Author Correction: Towards unifying fatty liver nomenclature: a voice from the Middle East and North Africa
Related Articles
Crosstalk between gut microbiotas and fatty acid metabolism in colorectal cancer
Colorectal cancer (CRC) is the third most common malignancy globally and the second leading cause of cancer-related mortality. Its development is a multifactorial and multistage process influenced by a dynamic interplay between gut microbiota, environmental factors, and fatty acid metabolism. Dysbiosis of intestinal microbiota and abnormalities in microbiota-associated metabolites have been implicated in colorectal carcinogenesis, highlighting the pivotal role of microbial and metabolic interactions. Fatty acid metabolism serves as a critical nexus linking dietary patterns with gut microbial activity, significantly impacting intestinal health. In CRC patients, reduced levels of short-chain fatty acids (SCFAs) and SCFA-producing bacteria have been consistently observed. Supplementation with SCFA-producing probiotics has demonstrated tumor-suppressive effects, while therapeutic strategies aimed at modulating SCFA levels have shown potential in enhancing the efficacy of radiation therapy and immunotherapy in both preclinical and clinical settings. This review explores the intricate relationship between gut microbiota, fatty acid metabolism, and CRC, offering insights into the underlying mechanisms and their potential translational applications. Understanding this interplay could pave the way for novel diagnostic, therapeutic, and preventive strategies in the management of CRC.
Cenozoic evolution of spring persistent rainfall in East Asia and North America driven by paleogeography
Spring persistent rainfall is a unique climate phenomenon that prevails in East Asia today, providing precious water resources to this densely populated region. However, its Cenozoic history and underlying mechanisms remain poorly understood. Here we show that the spring persistent rainfall in East Asia has emerged since the Miocene, whereas it previously flourished in North America during the Eocene, as revealed by climate models integrated with climate proxies. The contrasting evolution of spring persistent rainfall in East Asia and North America is determined by paleogeography and further influenced by CO2-induced warming. The uplift of the Tibetan Plateau and the westward drift of the Rocky Mountains have triggered a mid-latitude Rossby wave train since the Miocene, altering the position and intensity of the subtropical highs and thus rainfall patterns. Our results illuminate the Cenozoic evolution of spring persistent rainfall, with implications for the spring climate under the extreme future warming.
Toward change in the uneven geographies of urban knowledge production
More than four-fifths of the global urban population live in the Global South and East. Most urban theories, however, originate in the Global North. Building on recent efforts to address this mismatch, this paper examines the geographies of urban knowledge production. It analyzes the institutional affiliations of contributions in 25 leading Anglophone journals (n = 14,582) and nine urban handbooks (n = 252). We show that 42% of the journal articles and 17% of the handbook chapters were authored outside the Global North. However, only 15% of the editor positions (handbooks: 10%) were held by scholars based outside the Global North. This indicates that Global Northern institutions still dominate knowledge gatekeeping, whereas authors are more diverse. Additionally, more empirical journals and those with fewer Northern board members tend to publish more non-Northern authors. Our findings underscore the need for greater epistemic diversity in gatekeeping positions and broader understandings of what counts as theory to better incorporate diverse urban knowledge.
Activin E is a new guardian protecting against hepatic steatosis via inhibiting lipolysis in white adipose tissue
Hepatic endoplasmic reticulum (ER) stress is implicated in the development of steatosis and its progression to nonalcoholic steatohepatitis (NASH). The ER in the liver can sustain metabolic function by activating defense mechanisms that delay or prevent the progression of nonalcoholic fatty liver disease (NAFLD). However, the precise mechanisms by which the ER stress response protects against NAFLD remain largely unknown. Recently, activin E has been linked to metabolic diseases such as insulin resistance and NAFLD. However, the physiological conditions and regulatory mechanisms driving hepatic Inhbe expression (which encodes activin E) as well as the metabolic role of activin E in NAFLD require further investigation. Here we found that hepatic Inhbe expression increased under prolonged fasting and ER stress conditions, which was mediated by ATF4, as determined by promoter analysis in a mouse model. Consistently, a positive correlation between INHBE and ATF4 expression levels in relation to NAFLD status was confirmed using public human NAFLD datasets. To investigate the role of activin E in hepatic steatosis, we assessed the fluxes of the lipid metabolism in an Inhbe-knockout mouse model. These mice displayed a lean phenotype but developed severe hepatic steatosis under a high-fat diet. The deficiency of Inhbe resulted in increased lipolysis in adipose tissue, leading to increased fatty acid influx into the liver. Conversely, hepatic overexpression of Inhbe ameliorated hepatic steatosis by suppressing lipolysis in adipose tissue through ALK7–Smad signaling. In conclusion, activin E serves as a regulatory hepatokine that prevents fatty acid influx into the liver, thereby protecting against NAFLD.
SR-A3 suppresses AKT activation to protect against MAFLD by inhibiting XIAP-mediated PTEN degradation
Scavenger receptor class A member 3 (SR-A3) is implicated in metabolic diseases; however, the relationship between SR-A3 and metabolic dysfunction-associated fatty liver disease (MAFLD) has not been documented. Here, we show that hepatic SR-A3 expression is significantly reduced in human and animal models in the context of MAFLD. Genetic inhibition of SR-A3 in hamsters elicits hyperlipidemia, hyperglycemia, insulin resistance, and hepatic steatosis under chow-diet condition, yet escalates in diet-induced MAFLD. Mechanistically, SR-A3 ablation enhances E3 ligase XIAP-mediated proteasomal ubiquitination of PTEN, leading to AKT hyperactivation. By contrast, hepatic overexpression of human SR-A3 is sufficient to attenuate metabolic disorders in WT hamsters fed a high-fat-high-cholesterol diet and ob/ob mice via suppressing the XIAP/PTEN/AKT axis. In parallel, pharmacological intervention by PTEN agonist oroxin B or lipid lowering agent ezetimibe differentially corrects MAFLD in hamsters.
Responses