The Web of Science Core Collection included a total of 3,686 articles from 2002 to 2024, with the overall trend categorized into three phases. The initial phase spanned from 2003 to 2010, a stable period, and the annual publication volume remained basically at the same level. The second stage was from 2011 to 2020, a development period, and the overall trend of publication volume continued to rise. After 2020, the growth rate began to increase markedly and peaked in 2022 (399 articles), indicating that JAK1 research continues to attract the attention of researchers and has good development potential. See Figure 2A for details.

The top three research domains for JAK1 are oncology (642 articles), biochemistry (541 articles), and immunology (507 articles), collectively accounting for 46% of all JAK1-related publications. Figure 2B shows the top 10 research fields of JAK1 from 2002 to 2024: oncology, biochemistry, immunology, cell biology, pharmacology, hematology, medical research, medicine, chemistry, multidisciplinary science, and dermatology.

In total, 86 countries or regions have disseminated research papers on JAK1. We utilized Citespace software to construct a collaborative network of countries, as depicted in Figure 3A . Every node signifies a country. In the cooperation network of the issuing country, a larger node signifies a greater volume of documents dispatched by the country; a denser connection indicates a closer collaboration among entities. The connection line in the network signifies the collaboration between countries, while the line’s thickness denotes the degree of cooperation. Figure 3A illustrates that the United States and China are the foremost nations in JAK1 research, signifying their substantial influence in this domain and extensive collaboration with other countries. Figure 3B illustrates the top 10 countries by publication volume, which collectively represent 74% of the total publications, highlighting the concentration of nations engaged in JAK1-related research.

As shown in Figure 4 , a total of 199 institutions engaged in JAK1 research, with 6 institutions exhibiting centrality values of ≥0.1, indicating that multiple institutions are publishing key or transformative research. The University of California has the highest centrality (centrality = 0.38) as shown in Table 1 . The University of Texas has the most publications, followed by the French National Institute of Health and Medical Research, the University of California, the Icahn School of Medicine at Mount Sinai, Harvard University, Shanghai Jiao Tong University, the National Institutes of Health, the Paris Hospital Public Assistance (APHP), and the University of Paris. However, the collaboration between the main publishing institutions with the largest number of publications is weak.

We identified core authors using Price’s law. The calculation formula is N = 0.749 × η max , where ηmax represents the highest number of publications by an author, and authors with a publication count ≥N are considered core authors. Calculations reveal that the core author’s volume is ≥6 (5.554) articles, totaling 35 authors; The number of articles and the top 10 authors cited are shown in Table 2A , including Verstovsek, Srdan (55 articles), Ahn, KwangSeok (21 articles), Tanaka, Yoshiya (14 articles), Heinrich, PC (11 articles), Set Hi, Gautam (10 articles) is the top five authors in the volume of articles. The number of cited articles is the total number of cited articles for all articles published in the JAK1 research area by each author, as shown in Table 2B . The top five authors cited are OSHEAJJ (399 TIMES), VERSTOVSEKS (369 TIMES), QUINTÁS-CARDAMAA (234 TIMES), TEFFERIA (228 TIMES), and GHORESCHIK (213 TIMES).

Keywords typically serve to summarize and condense, thereby enhancing comprehension of the article’s principal themes. The literature keyword co-occurrence map ( Figure 5 ) comprises 174 nodes and 1461 links. The twenty most frequent keywords ( Table 3 ) pertain to mechanisms including gene expression (14), activation (15), pathways (16), and apoptosis (17), and are closely associated with diseases such as rheumatoid arthritis and cancer. They also encompass the analysis of safety and efficacy in clinical treatment. The keywords exhibiting a centrality exceeding 0.1 in the keyword co-occurrence analysis are expression (18), activation (19), cells (20), and rheumatoid arthritis (21), indicating that mechanistic research and rheumatoid arthritis are significant aspects of JAK1 research.

Utilizing the keyword co-occurrence map, the log-likelihood ratio (LLR) algorithm clusters the literature ( Figure 6 ), resulting in 13 cluster labels. The cluster labels of the literature keywords are: #0(srckinasesSRC), #1(psoriasis-likeinflammation), #2(poorprognosis), #3(atopicdermatitis), #4(jakactivityjak), #5(rheumatoidarthritis), #6(stat-3signalingpathway), #7(myeloproliferativeneoplasm), #8(potentialinhibitor), #9(polycythemiavera), #10(rig-iubiquitination), #11(triple-negativebreastcancer), #12(jak1-selectiveinhibitor).Clusters #0, #4, #6, and #10 primarily investigate the mechanism of JAK1; clusters #1, #3, #5, #7, #9, and #11 predominantly examine the disease spectrum of JAK1; clusters #8 and #12 chiefly focus on the clinical application of JAK1.

The literature cluster module value (Q)=0.7927(>0.3) signifies that the network structure of the cluster results is exceptional. The average contour value (S) serves as a metric for assessing the homogeneity of the network. A value approaching 1 indicates greater homogeneity within the network. If the value exceeds 0.7, it indicates that the cluster results are reliable. This study reveals that the average outline value for clustering in Chinese and English literature is 0.9374 (>0.7), signifying the credibility of the clustering results. The keyword cluster map of the literature indicates that each cluster overlaps and intersects, demonstrating the strong interconnection among them. The literature primarily focuses on the mechanistic research of JAK1 and the clinical investigation of surgical and tumor-associated diseases linked to skin inflammation.

A keyword timeline chart and highlight analysis facilitate comprehension of the research landscape in this domain and enable the identification of research trends. This study employs the keyword cluster map, utilizing the year as the horizontal axis and the cluster label as the vertical axis, to analyze the keyword timeline diagram using CiteSpace software ( Figure 7A ).

The keyword timeline diagram shows that the SRC kinase (cluster #0) has been widely studied since 2003. Atopic dermatitis (cluster #3) and JAK1-selective inhibitors (cluster #12) have become research hotspots in recent years. This implies that the main research focus and trend of JAK1 in the future will focus on clinical trials and mechanism research.

Keywords with the Strongest Citation Bursts refer to a significant increase in the frequency of a certain keyword in a short period, which indicates that research with high attention during this period can be used to determine hot spots and trends in the research field. “Begin” and “End” indicate the start and end time of Keywords with the strongest citation bursts, and “Strength” indicates the strength of Keywords with the strongest citation bursts. Increased strength correlates with enhanced influence.

Figure 7B shows the keywords with the strongest citation bursts analysis of JAK1 research literature. The top five keywords with the strongest citation bursts are polycythemiavera, myeloproliferativeneoplasms, geneexpression, signaltransduction, tyrosinekinasejak2. From the perspective of the length of highlight time, JAK1 literature research can be divided into three stages: from 2003 to 2009, the research focus was on the mechanism of JAK1; from 2008 to 2018, the main focus was on the combination of JAK1 and clinical diseases; from 2012 to 2024, the research focus began to shift to the development of JAK1 clinical drugs and their safety and efficacy.

Numerous studies have demonstrated that JAK1-related signaling pathways exhibit significant Anti-cancer efficacy (22, 23). The JAK/STAT signaling pathway suppresses the proliferation, differentiation, and apoptosis of tumor cells by inhibiting the activity of the suppressor of cytokine signaling (SOCS) family (24). In patients with colorectal cancer, JAK1 overexpression was significantly correlated with reduced survival, and the inhibition of JAK1 protein expression can impede cancer cell proliferation and progression, thereby effectively treating tumors (25). Moreover, JAK/STAT signaling pathways can combat cancer by modulating energy metabolism (26), influencing the immune microenvironment (27), and managing drug resistance (28), among other mechanisms.

Autophagy is the process of sending abnormal cell components in the body, such as unfolded proteins, aging and damaged cells, and accumulated harmful substances, to lysosomes or vesicles for digestion, degradation, and recycling. The occurrence of autophagy provides cells with the energy and environment needed for survival, which is a self-protection mechanism for somatic cells (29). The lack or overactivation of autophagy will cause the destruction of the normal structure of cells and cell death. Therefore, the balance of the autophagy process plays an important role in maintaining the stability of the intracellular environment (30). The JAK/STAT signaling pathway is an important pathway involved in autophagy. Many studies have shown (31, 32) that by inhibiting the expression of JAK/STAT-related signaling pathways, cancer cell autophagy can be regulated, thereby inhibiting the proliferation of cancer cells and achieving the purpose of inhibiting the malignant progression of cancer. Simultaneously, it modulates cellular autophagy through JAK/STAT-associated signaling pathways, which is significantly critical in diseases such as rheumatoid arthritis and diabetes (33, 34).

The JAK-STAT pathway is among the most expedited pathways in inflammation and serves as an essential pathway for inflammatory signaling (35). By inhibiting the activation of JAK/STAT-associated signaling pathways and modulating the release of various inflammatory mediators, it can ameliorate airway inflammation, influence skin barrier integrity, and restore the pathological condition of the gastric mucosa, thereby yielding a favorable therapeutic outcome for pulmonary disorders, inflammatory dermatoses, gastrointestinal ailments, and more (36–38).

Oxidative stress is a phenomenon of oxidation or imbalance in the body’s antioxidant system (39). When oxidation should be stimulated, the original redox dynamic balance in the cell is broken, resulting in the production of a large number of oxidation intermediate products, ROS, thus causing cell dysfunction and tissue organ damage. When the JAK1/STAT1 signaling pathway is inhibited, the oxidative stress response lobe is significantly inhibited, reducing brain tissue apoptosis, which reduces the apoptosis rate of neurons, plays a protective role in the brain, and is crucial in ischemia-reperfusion injury and many cardiovascular diseases (40).