INFLAMMATION RESEARCH
炎症研究
ISSN: 1023-3830
自引率: 1.2%
发文量: 96
被引量: 4185
影响因子: 6.979
通过率: 暂无数据
出版周期: 月刊
审稿周期: 4
审稿费用: 0
版面费用: 暂无数据
年文章数: 96
国人发稿量: 44

投稿须知/期刊简介:

Inflammation Research (IR) is an international journal which promptly publishes papers on all aspects of inflammation and related fields. Inflammation Research is the official journal of: The European Histamine Research Society (EHRS) The British Inflammation Research Association (BIRAs) The Inflammation Research Association (IRA) The Japanese Inflammation Society (JIS) The Canadian Inflammation Society (CIS) The types of papers published are original research papers short communications reviews commentaries selected reviewed society proceedings and meeting reports. In addition the journal publishes meeting reports letters opinions news of people policies and general information relating to the above fields of research and the societies active in these fields. Subject Coverage Histopathology immunological mechanisms gene expression mediators experimental models clinical investigations and the effects of drugs. Related fields are broadly defined and include for instance allergy and asthma shock pain joint damage skin disease as well as clinical trials of relevant drugs. Managing Editor and Editorial Office: Prof. M.J. Parnham PLIVA dd. Research Institute Prilaz baruna Filipovica 25 HR - 10000 Zagreb Croatia Tel.: ++385/1/378 1003 Fax: ++385/1/370 3175 e-mail:

期刊描述简介:

Inflammation Research (IR) is an international journal which promptly publishes papers on all aspects of inflammation and related fields. Inflammation Research is the official journal of: The European Histamine Research Society (EHRS) The British Inflammation Research Association (BIRAs) The Inflammation Research Association (IRA) The Japanese Inflammation Society (JIS) The Canadian Inflammation Society (CIS) The types of papers published are original research papers short communications reviews commentaries selected reviewed society proceedings and meeting reports. In addition the journal publishes meeting reports letters opinions news of people policies and general information relating to the above fields of research and the societies active in these fields. Subject Coverage Histopathology immunological mechanisms gene expression mediators experimental models clinical investigations and the effects of drugs. Related fields are broadly defined and include for instance allergy and asthma shock pain joint damage skin disease as well as clinical trials of relevant drugs. Managing Editor and Editorial Office: Prof. M.J. Parnham PLIVA dd. Research Institute Prilaz baruna Filipovica 25 HR - 10000 Zagreb Croatia Tel.: ++385/1/378 1003 Fax: ++385/1/370 3175 e-mail:

最新论文
  • Cyclic adenosine monophosphate critically modulates cardiac GLP-1 receptor's anti-inflammatory effects.

    被引量:- 发表:1970

  • The protective role of RACK1 in hepatic ischemia‒reperfusion injury-induced ferroptosis.

    被引量:- 发表:1970

  • Angiotensin-(1-7) decreases inflammation and lung damage caused by betacoronavirus infection in mice.

    被引量:- 发表:1970

  • Simultaneously blocking ANGPTL3 and IL-1β for the treatment of atherosclerosis through lipid-lowering and anti-inflammation.

    Blood lipid levels play a critical role in the progression of atherosclerosis. However, even with adequate lipid reduction, significant residual cardiovascular risk remains. Therefore, it is necessary to seek novel therapeutic strategies for atherosclerosis that can not only lower lipid levels but also inhibit inflammation simultaneously. The fusion protein FD03-IL-1Ra was designed by linking the Angiopoietin-like 3 (ANGPTL3) nanobody and human interleukin-1 receptor antagonist (IL-1Ra) sequences to a mutated human immunoglobulin gamma 1 (IgG1) Fc. This construct was transfected into HEK293 cells for expression. The purity and thermal stability of the fusion protein were assessed using SDS-PAGE, SEC-HPLC, and differential scanning calorimetry. Binding affinities of the fusion protein to ANGPTL3 and IL-1 receptor were measured using Biacore T200. The biological activity of the fusion protein was validated through in vitro experiments. The therapeutic efficacy of the fusion protein was evaluated in an ApoE-/- mouse model of atherosclerosis, including serum lipid level determination, histological analysis of aorta and aortic sinus sections, and detection of inflammatory and oxidative stress markers. ImageJ software was utilized for quantitative image analysis. Statistical analysis was performed using one-way ANOVA followed by Bonferroni post hoc test. The FD03-IL-1Ra fusion protein was successfully expressed, with no polymer formation detected, and it demonstrated good thermal and conformational stability. High affinity for both murine and human ANGPTL3 was exhibited by FD03-IL-1Ra, and it was able to antagonize hANGPTL3's inhibition of LPL activity. FD03-IL-1Ra also showed high affinity for both murine and human IL-1R, inhibiting IL-6 expression in A549 cells induced by IL-1β stimulation, as well as suppressing IL-1β-induced activity inhibition in A375.S2 cells. Our study revealed that the fusion protein effectively lowered serum lipid levels and alleviated inflammatory responses in mice. Furthermore, the fusion protein enhanced plaque stability by increasing collagen content within atherosclerotic plaques. These findings highlighted the potential of bifunctional interleukin-1 receptor antagonist and ANGPTL3 antibody fusion proteins for ameliorating the progression of atherosclerosis, presenting a promising novel therapeutic approach targeting both inflammation and lipid levels.

    被引量:- 发表:1970

  • Editorial expression of concern: Monocytes and lymphocytes as active participants in the pathogenesis of experimental shock.

    被引量:- 发表:1970

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