这几个地方理解的对吗？

The rapid kinetics of SARS-CoV replication and relative delay in type I IFN signaling may promote inflammatory M1 macrophage accumulation suggesting that targeted antagonism of this pathway would improve outcomes in patients with severe coronavirus infections [2]. Notably, the 2019 novel coronavirus (COVID-19) behaves more like SARS-CoV; accordingly it was named as SARS-CoV-2, progressing rapidly with acute respiratory distress syndrome (ARDS) and septic shock, which were eventually followed by multiple organ failure due to virus-induced cytokine storm in the body [4]. In response to infection macrophages must react rapidly with a substantial pro-inflammatory burst to kill microorganisms and to recruit additional immune cells to infection site. A sharp increase in the rate of glycolysis is closely associated with inflammatory phenotype in macrophages. Activated macrophages and effector T lymphocytes are shifted to the high glycolytic rate and high glucose uptake, even under oxygen-rich conditions, which is called as “Warburg effect”, upon immune activation, similar to cancer cells. Warburg effect is associated with diverse cellular processes, such as angiogenesis, hypoxia, polarization of macrophages, and activation of T cells. This phenomenon is intimately linked to several disorders, including sepsis, autoimmune diseases and cancer [5]. Another interesting aspect of glycolysis induction in activated immune cells is the role of the glycolytic enzyme, glyceraldehyde-3-phosphate dehydrogenase (GAPDH). It has been shown that GAPDH binds to the IFNγ coding mRNA, repressing its translation. However, GAPDH dissociates from IFNγ mRNA, allowing to its translation, upon glycolysis activation [6]. In addition, due to the glycolytic pathway stimulation in activated immune cells, their TCA becomes disrupted. Therefore, an accumulation of certain metabolites, including succinate, occurs. Succinate, in turn, may increase hypoxia-inducible factor-dependent activation of target genes, such as IL-1β and GLUT1 [7]. Glucose transporter, GLUT1, is required for the metabolic reprogramming, activation, and expansion of effector lymphocytes and M1 macrophages [7, 8].

SARS-CoV的快速复制和I型IFN信号传导的相对延迟可能促进炎性M1巨噬细胞聚集，提示该通路的靶向拮抗作用将改善严重冠状病毒感染患者的结局[2]。值得注意的是：2019年新型冠状病毒（COVID-19）的表现更像SARS-CoV，因此将其命名为SARS-CoV-2，如出现急性呼吸窘迫综合征（ARDS）和脓毒性休克COVID-19将进展迅速，并最终由于病毒诱导的体内细胞因子风暴而导致多器官衰竭[4]。在对感染的反应中，巨噬细胞必须以大量爆发的促炎因子的形式进行快速反应，以杀灭微生物并募集额外的免疫细胞至感染部位。糖酵解代谢的急剧增加与巨噬细胞的炎症表型（表达）密切相关。即使在富氧条件下，活化的巨噬细胞和效应T淋巴细胞在免疫激活后转至与癌细胞代谢相似的高糖酵解代谢和高葡萄糖摄取途径，也被称为“Warburg效应”。Warburg效应与多种细胞过程（如血管生成、缺氧、巨噬细胞极化和T细胞活化）相关，该现象也与多种疾病（包括脓毒症、自身免疫性疾病和癌症）密切相关[5]。另一个有趣的可激活免疫细胞糖酵解诱导的是糖酵解酶甘油醛-3-磷酸脱氢酶（GAPDH）的作用。研究表明GAPDH与IFNγ编码mRNA结合，抑制其翻译。然而，在糖酵解途径激活后GAPDH与IFNγmRNA解离，使其恢复翻译功能[6]。此外，由于活化的免疫细胞中的糖酵解途径刺激，其TCA被破坏，因此某些代谢物（包括琥珀酸盐）会发生蓄积。而琥珀酸盐反过来又可能激活靶基因增加缺氧依赖的诱导因子（如IL-1β和GLUT1）表达[7]，而葡萄糖转运蛋白GLUT1又是效应淋巴细胞和M1巨噬细胞代谢的重编程、活化和扩增所必需的[7,8]。

这几个地方翻译的对吗？

Succinate, in turn, may increase hypoxia-inducible factor-dependent activation of target genes, such as IL-1β and GLUT1。按翻译软件是：琥珀酸，反过来，可能增加缺氧诱导的因子依赖的靶基因的激活，如IL-1β和GLUT1。我总觉得不妥，应该按我上面的翻译（而琥珀酸盐反过来又可能激活靶基因增加缺氧依赖的诱导因子（如IL-1β和GLUT1）表达），对吗？如果对的，句子该如何分析成分？

phenotype表型？是不是就是表达的意思？或者就是 某种表型的高表达？