更新于：2024-05-01

SCARB1

清道夫受体B类成员-1

更新于：2024-05-01

基本信息

别名

CD36、CD36 and LIMPII analogous 1、CD36 antigen (collagen type I receptor, thrombospondin receptor)-like 1

+ [10]

简介

Receptor for different ligands such as phospholipids, cholesterol ester, lipoproteins, phosphatidylserine and apoptotic cells (PubMed:12016218, PubMed:12519372, PubMed:21226579). Receptor for HDL, mediating selective uptake of cholesteryl ether and HDL-dependent cholesterol efflux (PubMed:26965621). Also facilitates the flux of free and esterified cholesterol between the cell surface and apoB-containing lipoproteins and modified lipoproteins, although less efficiently than HDL. May be involved in the phagocytosis of apoptotic cells, via its phosphatidylserine binding activity (PubMed:12016218). (Microbial infection) Acts as a receptor for hepatitis C virus in hepatocytes and appears to facilitate its cell entry (PubMed:12356718, PubMed:12913001, PubMed:18000990). Binding between SCARB1 and the hepatitis C virus glycoprotein E2 is independent of the genotype of the viral isolate (PubMed:12356718). (Microbial infection) Mediates uptake of M.fortuitum, E.coli and S.aureus. (Microbial infection) Facilitates the entry of human coronavirus SARS-CoV-2 by acting as an entry cofactor through HDL binding.

关联

项与 SCARB1 相关的药物

ML279

靶点-

作用机制

SCARB1 抑制剂

在研机构

The Broad Institute, Inc.

原研机构

The Broad Institute, Inc.

在研适应症

心血管疾病

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

ML278

靶点-

作用机制

SCARB1 抑制剂

在研机构

One Cambridge Center Trust

原研机构

One Cambridge Center Trust

在研适应症

丙型肝炎

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

ITX-5061

靶点

SCARB1

作用机制

SCARB1拮抗剂

在研机构-

原研机构

iTherX Pharmaceuticals, Inc.

在研适应症-

非在研适应症

丙型肝炎 [+1]

最高研发阶段无进展

首次获批国家/地区-

首次获批日期1800-01-20

项与 SCARB1 相关的临床试验

NCT01560468 / Terminated临床1期IIT

Phase I Study of Hepatitis C Virus (HCV) Entry Inhibitor (ITX 5061) in Liver Transplant Recipients With HCV Infection

This study will test the safety and tolerability of HCV Entry Inhibitor ITX 5061 in Liver Transplant Recipients with Hepatitis C infection. The investigators hypothesize that ITX 5061 oral monotherapy will be safe in adults during and after liver transplantation and that therapy will also inhibit HCV infection of newly transplanted livers in adults with prior HCV infection.

开始日期2012-03-01

申办/合作机构

iTherX Pharmaceuticals, Inc.

NCT01292824 / Completed临床1期IIT

Phase I Study of Hepatitis C Virus (HCV) Entry Inhibitor (ITX 5061) in Liver Transplant Recipients With HCV Infection

This is a phase I pilot study to determine the safety and preliminary efficacy of a novel hepatitis C virus (HCV) entry inhibitor (ITX 5061) in patients with HCV infection undergoing liver transplantation.

开始日期2011-02-01

申办/合作机构

University of Birmingham

[+2]

NCT01165359 / Completed临床1期IIT

A Randomized, Double-Blind, Phase 1b Study to Assess the Safety and Activity of the HCV Entry Inhibitor ITX 5061 in Treatment-Naive HCV Mono-Infected Adults

Hepatitis C (HCV) is a disease that affects the liver. ITX 5061 is a new medication that is being tested to treat HCV. This study will evaluate the safety of ITX 5061 and examine different doses of the medication to evaluate which dose is the most effective at lowering the amount of HCV in the blood.

开始日期2010-09-01

申办/合作机构

National Institute of Allergy & Infectious Diseases

100 项与 SCARB1 相关的临床结果

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100 项与 SCARB1 相关的转化医学

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0 项与 SCARB1 相关的专利（医药）

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2,512

项与 SCARB1 相关的文献（医药）

2024-02-09·BMC cardiovascular disorders

Rare and common coding variants in lipid metabolism-related genes and their association with coronary artery disease.

Article

作者: Wei Li ; Yongyi Wang ; Ritai Huang ; Feng Lian ; Genxing Xu ; Weijun Wang ; Song Xue

BACKGROUND:

Coronary artery disease (CAD) is a complex disease that is influenced by environmental and genetic factors. In this study, we aimed to investigate the relationship between coding variants in lipid metabolism-related genes and CAD in a Chinese Han population.

METHODS:

A total of 252 individuals were recruited for this study, including 120 CAD patients and 132 healthy control individuals. Rare and common coding variants in 12 lipid metabolism-related genes (ANGPTL3, ANGPTL4, APOA1, APOA5, APOC1, APOC3, CETP, LDLR, LIPC, LPL, PCSK9 and SCARB1) were detected via next-generation sequencing (NGS)-based targeted sequencing. Associations between common variants and CAD were evaluated by Fisher's exact test. A gene-based association test of rare variants was performed by the sequence kernel association test-optimal (SKAT-O test).

RESULTS:

We found 51 rare variants and 17 common variants in this study. One common missense variant, LIPC rs6083, was significantly associated with CAD after Bonferroni correction (OR = 0.47, 95% CI = 0.29-0.76, p = 1.9 × 10^- 3). Thirty-three nonsynonymous rare variants were identified, including two novel variants located in the ANGPTL4 (p.Gly47Glu) and SCARB1 (p.Leu233Phe) genes. We did not find a significant association between rare variants and CAD via gene-based analysis via the SKAT-O test.

CONCLUSIONS:

Targeted sequencing is a powerful tool for identifying rare and common variants in CAD. The common missense variant LIPC rs6083 confers protection against CAD. The clinical relevance of rare variants in CAD aetiology needs to be investigated in larger sample sizes in the future.

2024-02-05·Nature communications

Resolvin T4 enhances macrophage cholesterol efflux to reduce vascular disease.

Article

作者: Mary E Walker ; Roberta De Matteis ; Mauro Perretti ; Jesmond Dalli

While cardiovascular disease (CVD) is one of the major co-morbidities in patients with rheumatoid arthritis (RA), the mechanism(s) that contribute to CVD in patients with RA remain to be fully elucidated. Herein, we observe that plasma concentrations of 13-series resolvin (RvT)4 negatively correlate with vascular lipid load in mouse inflammatory arthritis. Administration of RvT4 to male arthritic mice fed an atherogenic diet significantly reduces atherosclerosis. Assessment of the mechanisms elicited by this mediator demonstrates that RvT4 activates cholesterol efflux in lipid laden macrophages via a Scavenger Receptor class B type 1 (SR-BI)-Neutral Cholesterol Ester Hydrolase-dependent pathway. This leads to the reprogramming of lipid laden macrophages yielding tissue protection. Pharmacological inhibition or knockdown of macrophage SR-BI reverses the vasculo-protective activities of RvT4 in vitro and in male mice in vivo. Together these findings elucidate a RvT4-SR-BI centered mechanism that orchestrates macrophage responses to limit atherosclerosis during inflammatory arthritis.

2024-02-01·FASEB journal : official publication of the Federation of American Societies for Experimental Biology

Evidence for hypoxia-induced dysregulated cholesterol homeostasis in preeclampsia: Insights into the mechanisms from human placental cells and tissues.

Article

作者: Barbara Fuenzalida ; Maria Jose Yañez ; Martin Mueller ; Hiten D Mistry ; Andrea Leiva ; Christiane Albrecht

Preeclampsia (PE) poses a considerable risk to the long-term cardiovascular health of both mothers and their offspring due to a hypoxic environment in the placenta leading to reduced fetal oxygen supply. Cholesterol is vital for fetal development by influencing placental function. Recent findings suggest an association between hypoxia, disturbed cholesterol homeostasis, and PE. This study investigates the influence of hypoxia on placental cholesterol homeostasis. Using primary human trophoblast cells and placentae from women with PE, various aspects of cholesterol homeostasis were examined under hypoxic and hypoxia/reoxygenation (H/R) conditions. Under hypoxia and H/R, intracellular total and non-esterified cholesterol levels were significantly increased. This coincided with an upregulation of HMG-CoA-reductase and HMG-CoA-synthase (key genes regulating cholesterol biosynthesis), and a decrease in acetyl-CoA-acetyltransferase-1 (ACAT1), which mediates cholesterol esterification. Hypoxia and H/R also increased the intracellular levels of reactive oxygen species and elevated the expression of hypoxia-inducible factor (HIF)-2α and sterol-regulatory-element-binding-protein (SREBP) transcription factors. Additionally, exposure of trophoblasts to hypoxia and H/R resulted in enhanced cholesterol efflux to maternal and fetal serum. This was accompanied by an increased expression of proteins involved in cholesterol transport such as the scavenger receptor class B type I (SR-BI) and the ATP-binding cassette transporter G1 (ABCG1). Despite these metabolic alterations, mitogen-activated-protein-kinase (MAPK) signaling, a key regulator of cholesterol homeostasis, was largely unaffected. Our findings indicate dysregulation of cholesterol homeostasis at multiple metabolic points in both the trophoblast hypoxia model and placentae from women with PE. The increased cholesterol efflux and intracellular accumulation of non-esterified cholesterol may have critical implications for both the mother and the fetus during pregnancy, potentially contributing to an elevated cardiovascular risk later in life.

项与 SCARB1 相关的新闻（医药）

2023-09-16

·生物探索

非酒精性脂肪肝影响心血管疾病发生和进展的潜在机理

非酒精性脂肪性肝病(NAFLD)目前是一种日益增长的慢性流行病，并与心血管疾病(CVD)相关。然而，NAFLD如何影响CVD的发生和进展仍然不清楚。2023年9月4日，中山大学凌文华及广州医科大学Xue Hongliang共同通讯在Journal of Hepatology（IF=26）在线发表题为“Hepatic steatosis aggravates atherosclerosis via small extracellular vesicle-mediated inhibition of cellular cholesterol efflux”的研究论文，该研究表明肝脂肪变性通过小细胞外囊泡介导的抑制细胞胆固醇外排加重动脉粥样硬化。来自脂肪变性肝细胞的sEVs通过抑制ABCA在动脉粥样硬化进展中的作用。此外，肝细胞特异性缺失Rab27a可显著改善ApoE-/-小鼠高脂高胆固醇(HFHC)诱导的AS进展。Rab27a是调节sEVs释放的关键GTPase。miRNA深度测序结果显示，脂肪变性肝细胞的sEVs中富集了miR-30a-3p。miR-30a-3p直接靶向ABCA1 3'UTR抑制ABCA1表达和胆固醇外排。anagomiR-30a-3p治疗显著减轻HFHC喂养的ApoE-/-小鼠的动脉粥样硬化进展。此外，NAFLD患者血清sEVs降低了泡沫细胞中的胆固醇外排水平。sEV-miRNA-30a-3p相对含量与泡沫细胞胆固醇外排水平变化呈负相关。总之，脂肪变性肝细胞衍生的sEVs通过miR-30a-3p/ABCA1轴促进泡沫细胞形成和动脉粥样硬化。靶向和减少肝脏脂肪变性sEVs分泌或miR-30a-3p可能是减缓NAFLD驱动的AS进展的潜在治疗方法。久坐不动的生活方式和高热量食物的过度消费导致非酒精性脂肪性肝病(NAFLD)成为全球最普遍的肝病。有证据表明，NAFLD可影响包括心血管疾病(CVDs)在内的主要肝外代谢。肝脂肪变性与CVD和CVD相关事件的风险密切相关。动脉粥样硬化(AS)的发展和进展是心血管疾病的病理生理基础。然而，肝脂肪变性加速AS发展和进展的确切机制尚不清楚。细胞外囊泡(Extracellular vesicles，简称EVs)是源自供体细胞的膜状颗粒，可将其载货蛋白或miRNA运送到受体细胞，在代谢信号的器官间传递中发挥重要作用。作为细胞内通信的载体，EVs载货量可随着供体细胞受到的刺激而改变。小EVs通常指直径小于200 nm的EVs，其中包括外泌体和微泡。脂质超载后，肝细胞来源的sEVs在释放sEVs的数量和组成方面显示出巨大的变化。来自脂肪变性肝细胞的小EVs可加重肝脏炎症和NAFLD进展。然而，来自脂肪性肝细胞的sEVs是否会影响肝外代谢状况，尤其是AS，以及来自肝脂肪变性的细胞特异性信号如何调节AS进展仍然是悬而未决的问题。机理模式图（图源自Journal of Hepatology）动脉内膜中富含胆固醇的泡沫细胞是动脉粥样硬化进展的标志。动脉粥样硬化中泡沫细胞的主要细胞类型是巨噬细胞，巨噬细胞可以通过逆向胆固醇转运降低过量的细胞胆固醇水平 (RCT)。RCT的第一步是HDL通过ABCA1、ABCG1或SR-BI转运蛋白促进巨噬细胞的胆固醇外排，然后HDL-胆固醇被转运到肝脏排泄。越来越多的证据表明，巨噬细胞的RCT损伤会加剧AS的进展。该研究从脂肪变性肝细胞中分离了sEVs，并分析了这些sEVs在泡沫细胞形成和AS进展中的作用。研究结果表明，脂肪变性肝细胞来源的sEVs通过miR-30a-3p/ABCA1途径抑制巨噬细胞RCT，从而加剧泡沫细胞的形成和AS的进展，这表明抑制脂肪变性肝细胞的sEVs分泌或靶向miR-30a-3p可能能够改善NAFLD驱动的AS。此外，该研究肝脂肪变性在AS进展中的因果作用提供了概念验证的实验证据。总之，该研究揭示了肝脂肪变性通过sEVs在AS进展中的因果作用。来自脂肪变性肝细胞的sEVs可通过miR-30a-3p/ABCA1轴促进泡沫细胞形成。靶向和抑制sEVs分泌或miR-30a-3p可能是减轻NAFLD驱动的AS发展和进展的新治疗方法。文章来源“iNture”责编|文竞择校对|文竞择End往期精选围观历史性突破！不需卵子和精子就可以合成人类胚胎热文富豪用儿子血浆“回春”科学吗？Science：血液牛磺酸缺乏驱动衰老热文世界首例！35岁的她，通过机器人操刀移植的子宫，成功诞下宝宝热文为了避免心脏骤停，53岁的他成为“第一个”植入开创性除颤器的心脏病患者热文首次披露！175家生物制药公司的薪资数据：薪资中位数达20万美元点击“阅读原文”，了解更多~

临床研究临床结果

2023-09-03

·生物谷

研究发现高密度脂蛋白通过调控非编码RNA影响血管新生的新机制

冠心病是动脉粥样硬化导致冠状动脉狭窄和闭塞，引起心肌缺血、梗死的高死亡率心血管疾病。血管新生构建侧支循环对于心肌组织的血运重建十分重要。然而，冠心病状态下，多种危险因素持续损伤血管的功能，导致一系列促冠心病是动脉粥样硬化导致冠状动脉狭窄和闭塞，引起心肌缺血、梗死的高死亡率心血管疾病。血管新生构建侧支循环对于心肌组织的血运重建十分重要。然而，冠心病状态下，多种危险因素持续损伤血管的功能，导致一系列促进血管生长的措施没有疗效，其中一个关键因素是高密度脂蛋白(HDL)的功能障碍。正常HDL (nHDL)具有诱导血管新生的功能，但在冠心病等状态下，HDL的组分发生改变，导致诱导血管新生的功能丧失，甚至损伤血管新生，这种HDL称为失功能HDL(dHDL)。目前，对于dHDL为什么丧失诱导血管新生功能的机制尚未完全清楚。非编码RNA（Non-coding RNA）是指不编码蛋白质的RNA。其中包括微小RNA（miRNA），长链非编码RNA (lncRNA)等。这些RNA的共同特点是都能从基因组上转录而来，但是不翻译成蛋白，在RNA 水平上能行使各自的生物学功能了。其中lncRNA是一类大于200nt的非编码RNA，它的数量极其庞大，功能复杂多样，可调节血管细胞的增殖、衰老、凋亡等细胞活动，影响血管的生长和功能。我院区景松教授团队前期研究发现nHDL和dHDL诱导血管内皮细胞的lncRNA表达谱存在明显差异。然而，这些lncRNAs在nHDL和dHDL调节血管新生中的作用尚未清楚。2023年8月14日，中山大学附属第一医院区景松教授团队在Signal Transduction and Targeted Therapy 在线发表了题为“High-density lipoprotein regulates angiogenesis by long non-coding RNA HDRACA”的研究论文，首次发现nHDL通过抑制血管内皮细胞的lncRNA HDRACA表达来促进血管新生，而在冠心病状态下，dHDL对HDRACA的抑制明显减弱，导致dHDL丧失促进血管新生的功能。团队首先通过对lncRNA测序结果分析筛选，发现HDRACA可调节血管内皮细胞的增殖和管状形成，并确定了HDRACA是定位于内皮细胞浆中的长度553nt的无蛋白编码能力的lncRNA。进一步实验证实，nHDL可降低血管内皮细胞中的HDRACA表达，而dHDL对HDRACA表达的降低作用明显减弱。通过一系列分子实验发现，nHDL携带的S1P可与血管内皮细胞的S1P1相互作用诱导WWP2泛素连接酶磷酸化激活，催化HDRACA的转录因子KLF5泛素化降解，抑制HDRACA的转录。而dHDL携带的S1P含量明显减少，导致dHDL对HDRACA表达的抑制作用明显减弱。进一步实验证实nHDL抑制血管内皮细胞的HDRACA表达可促进血管新生，而dHDL对HDRACA表达的抑制明显减弱，导致它无法有效地促进血管新生。团队还发现HDRACA可以结合重要的血管新生调节蛋白RAIN，抑制RAIN和Vigilin的相互作用，进一步促进Vigilin诱导PCNA的mRNA不稳定降解，从而抑制PCNA的表达。nHDL通过抑制HDRACA表达影响RAIN-Vigilin-PCNA相互作用，促进PCNA的表达而促进血管新生。而dHDL无法有效地抑制HDRACA的表达，导致PCNA的表达减少，无法促进血管新生。该研究阐明了nHDL通过抑制lncRNA HDRACA表达促进血管新生，dHDL不能有效抑制lncRNA HDRACA表达而丧失诱导血管新生的作用和机制，为冠心病的血管新生治疗提供新的研究方向和靶点。 HDL通过调控lncRNA HDRACA影响血管新生此外，近年研究发现，HDL不但包含多种蛋白质和脂质，而且还携带非编码RNA，区景松教授团队发现，dHDL携带miRNA-24-3p明显nHDL多，nHDL可以通过HDL的经典受体SRB1抑制血管内皮细胞miRNA-24-3p的表达，从而使vinculin表达增多，激活PI3K-AKT-eNOS/ERK信号通路促进血管新生，但dHDL可以通过SRB1将携带的miRNA-24-3p导入血管内皮细胞，从而使vinculin表达下降，抑制PI3K-AKT-eNOS/ERK信号通路损伤血管新生。研究发现以题为“Angiogenic and antiangiogenic mechanisms of high density lipoprotein from healthy subjects and coronary artery diseases patients发表在期刊Redox Biology上。最近，区景松教授团队还发现HDL可以通过调控不同的miRNA影响血管新生。nHDL通过SRB1抑制另一个miR-181a-5p表达，使ATG5表达上调促进自噬，增强eNOS表达，增加内皮一氧化氮（NO）产生，诱导血管新生。 dHDL通过SRB1增强miR-181a-5p表达，抑制ATG5表达从而抑制自噬，下调eNOS表达，刺激氧自由基产生，损伤血管新生。通过过表达ATG5增加自噬可以恢复高胆固醇血症的血管新生。研究发现以文章题为：“High-density lipoprotein regulates angiogenesis by affecting autophagy via miRNA-181a-5p”于2023年6月20日在线发表在期刊Science China-Life Sciences上。综上，区景松教授团队近年来的研究系统地阐明了高密度脂蛋白通过调控非编码RNA影响血管新生的新机制, 为缺血性心脏病的血管新生治疗提供新的理论基础和治疗靶点。该研究得到国家重点研发计划项目、国家杰出青年科学基金、国家自然科学基金重大研究计划重点项目、国家自然科学基金重点项目、科技部国际重大合作项目等的联合资助。

2022-12-22

·佰傲谷BioValley

Efferocytosis：不同阶段分子差异与药物靶点

胞葬（Efferocytosis）是一种多阶段性的凋亡细胞清除机制，包括嗅觉阶段、吞噬阶段、消化阶段。各阶段的关键信号分子和相关信号通路可作为治疗胞葬异常性疾病的药物开发靶点。胞葬三阶段信号分子嗅觉阶段“find me”信号：凋亡细胞：核苷酸（ATP、UTP）、LPC、S1P、CX3CL1吞噬细胞：G2A、CX3CR1、LRP1、SRB1、P2Y2吞噬阶段“eat me”信号：凋亡细胞：PtdSer（PS）、氧化磷脂、内质网驻留钙蛋白吞噬细胞受体：TAM（Axl、Tyro3、MerTK）、TIM、TG2“don't eat me”信号：凋亡细胞：CD47、CD31吞噬细胞受体：SIRPα桥接分子：MFGE8、GAS6、ProS、血清补体C1q、Thbs1、AnxⅠ针对各阶段的治疗靶点嗅觉阶段嗅觉阶段功能正常发挥是胞葬顺利进行的关键，该阶段凋亡细胞表达的"find me"信号能够帮助吞噬细胞向凋亡细胞募集并增强其吞噬受体的表达。针对嗅觉阶段的体外光化学疗法（ECP）是基于提取光敏细胞作为理论基础的治疗方式。通过ECP将供体凋亡细胞处理后输入受体，能够激活吞噬阶段相关信号通路，有效治疗移植物抗宿主病（GVHD）。Nat Rev Drug Discov. 2022 Aug;21(8):601-620. 凋亡细胞代谢物可以用作药物来诱导修复和抗炎基因的表达，除GVHD外，输注凋亡细胞在治疗SLE、关节炎等炎症性疾病中具有很好的应用前景。吞噬阶段“eat me”信号磷酯酰丝氨酸（PS）是最典型的“eat me”信号，它的暴露并与TAM受体结合是该阶段的核心。PS其表达具有普遍性，多种疾病中这个过程发生异常，针对该异常情况是药物开发的重要靶点。ADAM对TAM受体（Axl、MerTK、Tyro）进行切割产生的sAxl、sMer、sTyro会使胞葬作用减弱，炎症程度增加。设计针对切割后产物的抗体能有效改善改善胞葬作用。Nat Rev Drug Discov. 2022 Aug;21(8):601-620. “don‘t eat me”信号CD47是经典的“don't eat me”信号，其表达上调会抑制对凋亡细胞的吞噬。靶向CD47-SIRP1α互作的抗体正在肿瘤中进行相关实验，对于动脉粥样硬化也可能具有一定治疗价值。Nat Rev Drug Discov. 2022 Aug;21(8):601-620. 凋亡细胞表面有多种“eat me”信号，通过与吞噬细胞表面受体特异性结合介导吞噬，针对受体的药物设计有以下思路：增加特定受体数量以增强吞噬效率工程化改造加强受体功能设计通用型booster，使炎症环境下能够促进PS受体扩增阻断或减少吞噬受体用于肿瘤治疗Nat Rev Drug Discov. 2022 Aug;21(8):601-620. 并且PS受体及CD47信号作为肿瘤治疗靶点已被广泛探索，目前多种药物在进行临床试验。clinicaltrials.gov消化阶段吞噬细胞摄入凋亡细胞后会面临极大的代谢负担，这就要求吞噬细胞细胞必须迅速清除内容物。而糖类、胆固醇、蛋白质、核酸等多种代谢物都会进入吞噬细胞的代谢循环，通过多种方式改变吞噬细胞的免疫代谢，也使吞噬细胞面临着表型被改变的挑战。以错综复杂的免疫-代谢网络作为靶点是针对该阶段药物开发的重点。Nat Rev Drug Discov. 2022 Aug;21(8):601-620. 用于治疗T2D的获批药物吡格列酮是PPARγ激动剂，能够通过PPARγ-LXRα-ABCA1通路促进胆固醇从凋亡细胞中排出以增强胞葬作用，在多种炎症性疾病中有很好的治疗前景。SLC家族负责代谢物的转运工作，SLC2a1能够促进葡萄糖摄取和增加糖酵解为胞葬提供能量。β-羟基丁酸能够增加SLC2a1的表达水平，将其作为膳食补充剂正在进行治疗T1D的临床试验（ NCT03999853 ）。参考资料DoranACetal. Efferocytosis in health and disease. Nat Rev Immunol. 2020 Apr;20(4):254-267. Zhang Yetal. Efferocytosis in multisystem diseases (Review). Mol Med Rep. 2022 Jan;25(1):13. MehrotraPetal. Drugging the efferocytosis process: concepts and opportunities. Nat Rev Drug Discov. 2022 Aug;21(8):601-620. Lin L et al. SLC transporters as therapeutic targets: emerging opportunities. Nat Rev Drug Discov. 2015 Aug;14(8):543-60.https://clinicaltrials.gov/近期热门视频更多精彩视频，尽在佰傲谷视频号，欢迎关注~本周好文推荐如需转载请联系佰傲谷并在醒目位置注明出处﹀点亮在看，传递信息♥