Very-low-density lipoprotein receptor-enhanced lipid metabolism in pancreatic stellate cells promotes pancreatic fibrosis

Yang, Xuguang; Chen, Jie; Wang, Jun; Ma, Shuai; Feng, Wenbo; Wu, Zhihao; Guo, Yangyang; Zhou, Hong; Mi, Wen-Li; Chen, Wei; Yin, Bo; Lin, Yu‐Li

doi:10.1016/j.immuni.2022.06.001

Cited by 39 publications

(15 citation statements)

References 54 publications

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“…Very-low-density lipoproteins (VLDL) are a risk factor for modic changes. These changes result in low back pain (LBP), and receptors can enhance lipid metabolism and promote the expression of interleukin-33 (IL-33) [ 9 , 52 ]. More studies are needed, however, to investigate the relationship between lipid metabolism and metabolite metabolism in the process of MT or TE in reducing cNLBP.…”

Section: Discussionmentioning

confidence: 99%

Lipid and metabolic alteration involvement in physiotherapy for chronic nonspecific low back pain

Zhang

et al. 2022

Lipids Health Dis

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Background Chronic nonspecific low back pain (cNLBP) is a common health problem worldwide, affecting 65–80% of the population and greatly affecting people’s quality of life and productivity. It also causes huge economic losses. Manual therapy (MT) and therapeutic exercise (TE) are effective treatment options for cNLBP physiotherapy-based treatment. However, the underlying mechanisms that promote cNLBP amelioration by MT or TE are incompletely understood. Methods Seventeen recruited subjects were randomly divided into an MT group and a TE group. Subjects in the MT group performed muscular relaxation, myofascial release, and mobilization for 20 min during each treatment session. The treatment lasted for a total of six sessions, once every two days. Subjects in the TE group completed motor control and core stability exercises for 30 min during each treatment session. The motor control exercise included stretching of the trunk and extremity muscles through trunk and hip rotation and flexion training. Stabilization exercises consisted of the (1) bridge exercise, (2) single-leg-lift bridge exercise, (3) side bridge exercise, (4) two-point bird-dog position with an elevated contralateral leg and arm, (5) bear crawl exercise, and (6) dead bug exercise. The treatment lasted for a total of six sessions, with one session every two days. Serum samples were collected from subjects before and after physiotherapy-based treatment for lipidomic and metabolomic measurements. Results Through lipidomic analysis, we found that the phosphatidylcholine/phosphatidylethanolamine (PC/PE) ratio decreased and the sphingomyelin/ceramide (SM/Cer) ratio increased in cNLBP patients after MT or TE treatment. In addition, eight metabolites enriched in pyrimidine and purine differed significantly in cNLBP patients who received MT treatment. A total of nine metabolites enriched in pyrimidine, tyrosine, and galactose pathways differed significantly in cNLBP patients after TE treatment during metabolomics analysis. Conclusion Our study was the first to elucidate the alterations in the lipidomics and metabolomics of cNLBP physiotherapy-based treatment and can expand our knowledge of cNLBP physiotherapy-based treatment.

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Section: Discussionmentioning

confidence: 99%

Lipid and metabolic alteration involvement in physiotherapy for chronic nonspecific low back pain

Zhang

et al. 2022

Lipids Health Dis

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“…[41,42] This shows that even in the same disease, these cells can differentially respond to microenvironmental cues and have different consequences on pathogenesis through either direct influence on tumor cells themselves or indirectly through interaction with immune cells. While studies have focused on understanding the heterogeneous responses PaSCs transition through in adult disease states including pancreatitis and pancreatic cancer, [43][44][45] the functional significance and developmental relationship of PaSCs during organogenesis and cellular maturation are largely overlooked. As these cells constantly monitor their environment and rapidly transition from "quiescence" into an activated state, it is reasonable to speculate that these cells are also highly active throughout the massive changes occurring during tissue formation and development.…”

Section: Pancreatic Mesenchyme Dynamically Changes Over Developmentmentioning

confidence: 99%

Deep into the niche: Deciphering local endoderm‐microenvironment interactions in development, homeostasis, and disease of pancreas and intestine

et al. 2023

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Unraveling molecular and functional heterogeneity of niche cells within the developing endoderm could resolve mechanisms of tissue formation and maturation. Here, we discuss current unknowns in molecular mechanisms underlying key developmental events in pancreatic islet and intestinal epithelial formation. Recent breakthroughs in single‐cell and spatial transcriptomics, paralleled with functional studies in vitro, reveal that specialized mesenchymal subtypes drive the formation and maturation of pancreatic endocrine cells and islets via local interactions with epithelium, neurons, and microvessels. Analogous to this, distinct intestinal niche cells regulate both epithelial development and homeostasis throughout life. We propose how this knowledge can be used to progress research in the human context using pluripotent stem cell‐derived multilineage organoids. Overall, understanding the interactions between the multitude of microenvironmental cells and how they drive tissue development and function could help us make more therapeutically relevant in vitro models.

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“…Although LPL expression in the pancreas is relatively low, evidence indicates that elevated VLDL levels contribute to the development of pancreatitis, as a common condition among obese and T2D patients [ 41 , 42 ], and are further known to be associated with fatty liver disease [ 43 ]. In mice, deletion of the VLDLR in pancreatic stellate cells ameliorates the development of pancreatitis [ 44 ].…”

Section: Liver-derived Lipids As Signaling Moleculesmentioning

confidence: 99%

Liver-derived metabolites as signaling molecules in fatty liver disease

Keles

Kuentzel

et al. 2022

Cell. Mol. Life Sci.

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Excessive fat accumulation in the liver has become a major health threat worldwide. Unresolved fat deposition in the liver can go undetected until it develops into fatty liver disease, followed by steatohepatitis, fibrosis, cirrhosis, and eventually hepatocellular carcinoma. Lipid deposition in the liver is governed by complex communication, primarily between metabolic organs. This can be mediated by hormones, organokines, and also, as has been more recently discovered, metabolites. Although how metabolites from peripheral organs affect the liver is well documented, the effect of metabolic players released from the liver during the development of fatty liver disease or associated comorbidities needs further attention. Here we focus on interorgan crosstalk based on metabolites released from the liver and how these molecules act as signaling molecules in peripheral tissues. Due to the liver’s specific role, we are covering lipid and bile mechanism-derived metabolites. We also discuss the high sucrose intake associated with uric acid release from the liver. Excessive fat deposition in the liver during fatty liver disease development reflects disrupted metabolic processes. As a response, the liver secretes a variety of signaling molecules as well as metabolites which act as a footprint of the metabolic disruption. In the coming years, the reciprocal exchange of metabolites between the liver and other metabolic organs will gain further importance and will help to better understand the development of fatty liver disease and associated diseases.

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Very-low-density lipoprotein receptor-enhanced lipid metabolism in pancreatic stellate cells promotes pancreatic fibrosis

Cited by 39 publications

References 54 publications

Lipid and metabolic alteration involvement in physiotherapy for chronic nonspecific low back pain

Lipid and metabolic alteration involvement in physiotherapy for chronic nonspecific low back pain

Deep into the niche: Deciphering local endoderm‐microenvironment interactions in development, homeostasis, and disease of pancreas and intestine

Liver-derived metabolites as signaling molecules in fatty liver disease

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