Evolutionary trend analysis and knowledge structure mapping of endothelial dysfunction in sepsis: a bibliometrics study

doi:10.5847/wjem.j.1920-8642.2024.083

Abstract

Abstract:

BACKGROUND A pathophysiological feature of septic organ failure is endothelial dysfunction in sepsis (EDS). The physiological and pathological mechanism of sepsis is considered to be vascular leakage caused by endothelial dysfunction. These pathological changes lead to systemic organ injury. However, an analysis using bibliometric methods has not yet been conducted in the field of EDS. This study was conducted to provide an overview of knowledge structure and research trends in the field of EDS.

METHODS Based on previous research, a literature search was performed in the Web of Science Core Collection (WoSCC) for publications associated with EDS published between the year 2003 and 2023. Various types of data from the publications, such as citation frequency, authorship, keywords and highly cited articles, were extracted. The "Create Citation Report" feature in the WoSCC was employed to calculate the Hirsch index (h-index) and average citations per item (ACI) of authors, institutions, and countries. To conduct bibliometric and visualization analyses, three bibliometric tools were used, including R-bibliometrix, CiteSpace (co-citation analysis of references), and VOSviewer (co-authorship analysis of institutions, co-authorship analysis of authors, co-occurrence analysis of keywords).

RESULTS After excluding invalid records, the study finaly included 4,536 publications with 135,386 citations. Most of these publications originated in the USA, China, Germany, Canada, and Japan. Harvard University emerged as the most prolific institution, while professor Jong-Sup Bae and his research team at Kyungpook National University emerged as authors with the greatest influence. The "protein C", "tissue factor", "thrombin", "glycocalyx", “acute kidney injury”, “syndecan-1” and “biomarker” were identified as prominent areas of research. Future research may focus on molecular mechanisms (such as as vascular endothelial [VE]-cadherin regulation) and therapeutic interventions to enhance endothelial repair and function.

CONCLUSION Our findings show a growing interest in EDS research. Key areas for future research include signaling pathways, molecular mechanisms, endothelial repair, and interactions between endothelial cells and other cell types in sepsis.

Key words: Sepsis, Endothelium, Bibliometrics, CiteSpace, VOSviewer

Juexian Wei, Hengzong Mo, Yuting Zhang, Wenmin Deng, Siqing Zheng, Haifeng Mao, Yang Ji, Huilin Jiang, Yongcheng Zhu. Evolutionary trend analysis and knowledge structure mapping of endothelial dysfunction in sepsis: a bibliometrics study[J]. World Journal of Emergency Medicine, 2024, 15(5): 386-396.

Figures/Tables 10

Figure 1.

Table 1.

Figure 2.

Figure 3.

Figure 4.

Table 2.

The top 20 most cited publications about endothelial dysfunction in sepsis

Rank	Title	First author	Corresponding author	Journal	Publication year	Total citations
1	Cellular pathophysiology of ischemic acute kidney injury	Bonventre JV	Bonventre JV	Journal of Clinical Investigation	2011	1,406
2	Extracellular histones are major mediators of death in sepsis	Xu J	Esmon CT	Nature Medicine	2009	1,122
3	The role of adherent junctions and VE-cadherin in the control of vascular permeability	Dejana E	Dejana E	Journal of Cell Science	2008	743
4	Toll-like receptors in the pathogenesis of human disease	Cook DN	Cook DN	Nature Immunology	2004	678
5	Inflammation-promoting activity of HMGB1 on human microvascular endothelial cells	Fiuza C	Suffredini AF	Blood	2003	632
6	The protein C pathway	Esmon CT	Esmon CT	Chest	2003	615
7	The pulmonary endothelial glycocalyx regulates neutrophil adhesion and lung injury during experimental sepsis	Schmidt EP	Schmidt EP	Nature Medicine	2010	574
8	Allogeneic human mesenchymal stem cells for treatment of E. coli endotoxin-induced acute lung injury in the ex vivo perfused human lung	Lee JW	Lee JW	Proceedings of the National Academy of Sciences of the United States of America	2008	558
9	A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation	Erridge C	Erridge C	American Journal of Clinical Nutrition	2004	557
10	Resolvin D2 is a potent regulator of leukocytes and controls microbial sepsis	Spite M	Serhan CN	Nature	2003	537
11	Comprehensive human cell-type methylation atlas reveals origins of circulating cell-free DNA in health and disease	Moss J	Shemer R & Dor Y	Nature Communications	2003	507
12	Activated protein C blocks p53-mediated apoptosis in ischemic human brain endothelium and is neuroprotective	Cheng T	Zlokovic BV	Nature Medicine	2003	501
13	Complete reversal of acid-induced acute lung injury by blocking of platelet-neutrophil aggregation	Zarbock A	Ley K	Journal of Clinical Investigation	2010	485
14	The systemic immune response to trauma: an overview of pathophysiology and treatment	Lord JM	Lilford RJ	Lancet	2009	479
15	Inflammation, endothelium, and coagulation in sepsis	Schouten M	van der Poll T	Journal of Leukocyte Biology	2009	477
16	Receptor for advanced glycation end products (RAGE) regulates sepsis but not the adaptive immune response	Liliensiek B	Nawroth PP	Journal of Clinical Investigation	2004	439
17	Ghrelin inhibits proinflammatory responses and nuclear factor-κB activation in human endothelial cells	Li WG	Weintraub NL	Circulation	2004	438
18	MicroRNA-181b regulates NF-κB-mediated vascular inflammation	Sun XH	Feinberg MW	Journal of Clinical Investigation	2012	433
19	Immunologic and hemodynamic effects of “low-dose” hydrocortisone in septic shock - A double-blind, randomized, placebo-controlled, crossover study	Keh D	Keh D	American Journal of Respiratory and Critical Care Medicine	2003	422
20	Endothelial barrier protection by activated protein C through PAR1-dependent sphingosine 1-phosphate receptor-1 cross activation	Feistritzer C	Riewald M	Blood	2005	414

Table 2.

Table 3.

Figure 5.

Figure 6.

Figure 7.

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Rank	Country	Publications	% of 4,536	Times cited	ACI	h-index	Betweenness centrality
1	USA	1,550	34.2	68,956	44.49	112	0.08
2	China	914	20.2	15,402	16.85	60	0.04
3	Germany	543	12.0	18,281	33.67	61	0.08
4	Canada	277	6.1	12,334	44.53	56	0.14
5	Japan	274	6.0	7,353	26.84	44	0
6	Netherlands	230	5.1	8,404	36.54	51	0.16
7	France	207	4.6	9,005	43.29	42	0.08
8	England	207	4.6	7,612	36.77	44	0.36
9	South Korea	185	4.1	3,375	18.24	35	0
10	Brazil	147	3.2	4,064	27.65	34	0.04
11	Italy	128	2.8	4,344	33.94	32	0.52
12	Spain	103	2.3	3,200	31.07	28	0.63
13	Sweden	95	2.1	2,998	31.56	23	0.24
14	Türkiye	80	1.8	975	12.04	15	0
15	Australia	80	1.8	2,200	27.50	33	0.15
16	Belgium	80	1.8	4,114	51.43	25	1.03
17	Switzerland	74	1.6	3,300	44.00	27	0.04
18	Austria	73	1.6	2,076	28.44	24	0
19	Denmark	59	1.3	1,545	26.19	21	0.04
20	India	47	1.0	728	15.49	14	0.03

Cluster ID	Size	Silhouette	Label	Mean (year)
#0	101	0.946	Protein C	2003
#1	86	0.904	Endothelial glycocalyx	2016
#2	67	0.898	Angiogenic factor	2008
#3	49	0.998	HMGB1-induced inflammatory responses	2012
#4	48	0.889	Host response	2013
#5	46	0.933	COVID-19 coagulopathy	2019
#6	43	0.899	Sepsis-induced acute lung Injury	2018
#7	31	0.933	Microcirculatory dysfunction	2004
#8	29	0.979	Endothelial damage	2009
#9	12	0.986	Acute lung injury	2011
#10	11	0.979	Inhibitory function	2016
#11	6	0.995	Prostacyclin production	2000
#13	6	0.996	Endothelial activation dysfunction	2007
#14	6	0.940	Protein response	2019

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