Global Research Trends in Oxidative Stress and Myocardial Fibrosis: A Dual-Software Bibliometric Study

Introduction

MF is a common pathological change in the development of various cardiovascular diseases, characterized by the pathological remodeling of the ECM.¹ Persistent fibrosis can affect myocardial metabolism, reduce tissue compliance, lead to ventricular remodeling, and accelerate the progression to heart failure (HF).^2,3 Globally, the annual incidence rate of MF is approximately 1.7%. Notably, the progression of MF to HF is associated with a significantly elevated mortality risk, with 5-year mortality rates ranging from 40% to 60%.⁴ How to effectively prevent and delay fibrosis is a hot and challenging issue in the treatment of HF. Modern medicine posits that the pathogenesis of MF is associated with the continuous activation of the Renin-Angiotensin-Aldosterone System (RAAS), inflammatory responses, and autophagy. Clinically, treatments for MF include RAAS inhibitors, beta-blockers, and statins. These medications can alleviate clinical symptoms in patients but have limited effects in halting or reversing MF. When patients discontinue these medications or develop drug tolerance, their conditions may deteriorate further.^5,6 Multiple studies have shown that oxidative stress is an important factor in promoting the occurrence and development of MF, so how oxidative stress plays a role in the different stages of MF development has increasingly attracted the attention of researchers.

Oxidative stress refers to the abnormal metabolic state caused by an imbalance between the oxidative and antioxidant systems in the body, resulting in the accumulation of large amounts of reactive oxygen species (ROS) and reactive nitrogen species (RNS) under the stimulation of various harmful factors.^7,8 In a physiological state, low levels of ROS and RNS are necessary signaling molecules for mediating cell signal transduction and maintaining the body’s balance. However, the excessive production of ROS and RNS can lead to an oxidative stress response, causing the denaturation of proteins, lipids, DNA, and RNA, thereby damaging myocardial cells.⁹ Increasing research has shown that oxidative stress plays an important role in multiple stages of the development of MF, mainly related to the induction of myocardial cell apoptosis, the promotion of inflammatory factor expression, and the abnormal proliferation of cardiac fibroblasts (CFs) leading to ECM remodeling.⁹ Therefore, alleviating oxidative stress is an effective strategy to inhibit inflammation and MF.

CiteSpace, developed by Professor Chaomei Chen at Drexel University in the United States, is a widely recognized bibliometric software that has garnered substantial attention from both domestic and international scholars in recent years.^10–12 This software is uniquely equipped to systematically trace hidden patterns and associations within extensive document collections. By analyzing key indicators such as the volume of literature output, author collaboration networks, co-occurrence of keywords, and citation trajectories, CiteSpace not only quantifies the development trends of research topics but also uncovers latent knowledge structures that traditional review methods might overlook.^10–12 However, CiteSpace is not the only tool available in this domain. VOSviewer, developed by Van Eck and Waltman at Leiden University in the Netherlands, is another powerful bibliometric mapping tool.¹³ It excels in generating various visualizations based on bibliometric relationships, such as co-citation networks of authors or journals and co-occurrence networks of keywords. Consequently, this tool is particularly useful for revealing the structure, evolution, and collaboration within a knowledge domain. In the early stages of COVID-19 research, bibliometric analysis unexpectedly revealed that the academic attention given to Remdesivir far exceeded the level of clinical evidence supporting its efficacy. This “premature focus” in the academic community not only exposed the collective cognitive bias of the scientific community towards potential therapies during public health crises but also directly propelled discussions on the paradigm of evidence weighting and resource allocation principles in research on emerging infectious diseases. Thus, while CiteSpace and VOSviewer offer valuable insights into research trends and knowledge structures, their findings also highlight the importance of aligning academic attention with robust clinical evidence, particularly in the context of public health emergencies.¹⁴ Therefore, this study used CiteSpace 6.3.R2 and VOSviewer 1.6.20 to visualize the knowledge maps of literature on oxidative stress related to MF in the Web of Science database, and conducted bibliometric analysis, in order to demonstrate the current research status, development trajectory, research hotspots, and potential trends, with the aim of providing reference and inspiration for future related research.

Data and Methods

Data Sources and Search Strategy

The Web of Science Core Collection (WoSSC) provides a comprehensive overview of relevant information, including publications, citations, authors, references, and keywords, making it one of the most widely used databases in bibliometric research.¹⁵ This study used WoSSC as the data source for the basic search, with the search terms TS = (“Oxidative Stress” OR “Antioxidative Stress”) AND TS = (“myocardial fibrosis” OR “myocardial interstitial fibrosis” OR “cardiac fibrosis” OR “atrial fibrosis” OR “ventricular fibrosis” OR “heart fibrosis” OR “myocard* fibrosis” OR “myocard* interstitial fibrosis” OR “card* fibrosis”), limiting the publication time from the database inception to December 31, 2024, and the document types to “Article” and “Review”, with the language limited to “English”. The search was conducted on December 31, 2024, and irrelevant literature was excluded. The full records (including title, author, source, abstract, keywords, cited references, and publication year) were exported in text format for analysis, and named in the format “download_**.txt”. Furthermore, to ensure the accuracy and reliability of the research data, two researchers independently completed the data collection and screening tasks, and a third person was involved to make the final decision if there were any disagreements.

Analysis Methods

Using the VOSviewer software, author and institution collaboration network maps were created. Based on CiteSpace 6.3.R2 software, visualization analyses were conducted for countries and keywords, to analyze the current research status, frontiers, and development trends of oxidative stress related to MF.

Results

Distribution of Literature

An analysis was conducted on the 1,831 included articles, and a flowchart was created, as shown in Figure 1. The annual publication trend was plotted, as shown in Figure 2. From the figure, it can be seen that research on oxidative stress related to MF first appeared in 1999, and the publication volume has slowly increased since then. 2014 was a turning point, global publications increased at a compound annual growth rate (CAGR) of 16.0%, after which the publication volume began to grow rapidly, reaching a historical high in 2022. Overall, the publication volume on the topic of oxidative stress in MF research has shown a stable growth trend, reflecting the immense development potential and prospect of this research field.

Figure 1 Flowchart for incorporating articles.

Figure 2 Trend of annual publication volume.

Collaborative Network Analysis

Distribution of Authors

The visualization map can provide information on influential research teams and potential collaborators, and can help researchers establish collaborative relationships.¹⁶ The 1,831 articles involved 215 authors, with the most prolific author being Sowers, James R (19 articles). The top 10 authors by publication volume are shown in Table 1. Using VOSviewer, an author collaboration network map was generated, as shown in Figure 3. Overall, the collaboration relationships among scholars are relatively close. By analyzing the author collaboration relationships, it can be seen that several major research teams have taken shape around Sowers, James R, Young, Morag J, Cachofeiro, Victo, Wang, Jing, and others, indicating that they have made important contributions to the research on the role of oxidative stress in MF.

Table 1 Authors with a Publication Frequency of ≥11

Figure 3 Author collaboration chart.

Distribution of Countries/Institutions

Analyzing the distribution of authors’ countries/institutions can help understand the research enthusiasm of various countries and institutions in the field of oxidative stress related to MF. CiteSpace software and VOSviewer were used to generate country co-occurrence maps and institution co-occurrence maps, respectively. The results of this study show that 66 countries have participated in the related research on oxidative stress in MF, and the distribution of the top 10 countries/regions by publication volume is shown in Table 2.

Table 2 Number of National Publications

The top 10 countries are mainly distributed in North America, Asia, and Europe. The country with the most published papers is China (n = 690, 39.32%), followed by the United States (n = 451, 25.70%). China and the United States account for more than half of the total publications, indicating that these two countries have invested relatively more research funding and personnel in the field of oxidative stress in MF, which also reflects that economic development is the basis for driving disease prevention and health development.

We have constructed a time zone map according to the publication time order of the 66 countries, as shown in Figure 4. From Figure 4, we can see that China started relatively late in this field, but with the rapid economic development and the continuous increase in research investment, China’s academic contribution in this field has made significant progress and has become one of the countries with the most publications in this field. In addition, the cooperation among countries is quite close. For example, the United States cooperates closely with Australia and Canada; China cooperates more with the United States and the United Kingdom.

Figure 4 Research country co-occurrence map.

The institution collaboration map is shown in Figure 5, and the top 10 institutions by publication volume are shown in Table 3, which are Shandong University (China; n = 42), Nanjing Medical University (China; n = 38), Shanghai Jiao Tong University (China; n = 36), Wuhan University (China; n = 35), Monash University (Australia; n = 30), Fudan University (China; n = 27), Capital Medical University (China; n = 26), University of Missouri (USA; n = 26), China Medical University (China; n = 23), and China Academy of Chinese Medical Sciences (China; n = 23). Among them, Chinese institutions occupy 8 places, suggesting that China is active in the research on oxidative stress in MF, indicating that Chinese researchers have invested a great deal of effort and resources in this field, and have played an important role in the construction of the global scientific knowledge system in this field.

Table 3 Top 10 Research Institutions in Terms of the Number of Publications and Centrality

Figure 5 Mapping of institutional cooperation.

Number of Journal Publications

Through the analysis of the published journals, the important journal sources and characteristics of the literature on oxidative stress related to MF can be revealed. There are a total of 13 journals with more than 20 publications, as shown in Table 4. Among them, “INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES” reported the most in this field, with 42 papers. “CARDIOVASCULAR RESEARCH” has the highest impact factor (IF = 10.9), indicating that the quality and academic impact of research papers in this field have received attention and recognition from authoritative international journals.

Table 4 Number of Journal Articles

Keyword Analysis

Keyword Co-Occurrence Analysis

Co-occurrence keywords can reflect the core research content of the research field of oxidative stress related to MF, that is, the research hotspots. As shown in Figure 6, the co-occurrence keyword map was obtained, and combined with the analysis of Table 5, the top 20 keywords with the highest frequency in this field are oxidative stress, MF, heart failure, cardiac hypertrophy, dysfunction, expression, activation, etc. A comprehensive analysis of the above keywords reveals that the research hotspots in the field of oxidative stress-related MF research are mainly focused on: The regulatory mechanisms of oxidative stress in MF caused by different etiologies (heart failure, myocardial infarction, diabetic cardiomyopathy, cardiomyopathy, atrial fibrillation); The biological processes that coexist in MF oxidative stress, such as inflammation, apoptosis, injury, and dysfunction; The substances involved in regulating the oxidative stress process in MF, such as angiotensin II, NADPH oxidase, NF-κB, etc.

Table 5 High-Frequency Keywords

Figure 6 Keyword co-occurrence mapping.

Keyword Clustering Analysis

After running Citespace for keyword clustering analysis, a keyword clustering peak-valley map was obtained, as shown in Figure 7. Based on the keyword clustering map, the research on oxidative stress related to MF can be divided into nine major clusters: glucocorticoid receptor, reperfusion injury, diabetic cardiomyopathy, MF, atrial fibrillation, cardiovascular disease, protein kinase C (PKC), dilated cardiomyopathy, and ECM. The nine major research directions of oxidative stress related MF research are summarized based on the keywords in each cluster, as shown in Table 6.

Table 6 Clustering Labels

Figure 7 Keyword clustering.

Keyword Mutation Analysis

Burst keywords are words whose frequency change rate is relatively high during a certain period, which can reflect the research frontiers and the evolution of research topics over the years. Using the Burstness function in CiteSpace, it can be seen from Figure 8 that the early and long-lasting burst keywords were found to be “tumor necrosis factor α”, “angiotensin converting enzyme”, “nitric oxide synthase”, and “gene expression”. The longest-lasting burst was “gene expression” at 15 years. Keywords with burst strength greater than 10 include “angiotensin II”, “glucocorticoid receptor”, “NADPH oxidase”, and “blood pressure”, with “angiotensin II” having the highest burst strength of 19.43 and lasting for 10 years. A recent burst keyword is “NLRP3 inflammasome”, which suggests that researchers in this field believe oxidative stress can activate the NLRP3 inflammasome signaling pathway to promote the development of MF. This indicates that research on inflammation-related signaling pathways will be a key focus in the future of oxidative stress in MF.

Figure 8 Keyword burst.

Co-Citation Analysis of Journals

The knowledge flow analysis method was used to explore the evolution of journal citations and co-citations.¹⁶ The journal’s dual-map overlay shows the distribution of academic journal topics, changes in citation trajectories, and the transfer of research centers. The left-hand labels of the dual-map represent the citing fields, and the right-hand labels represent the cited fields.¹⁷ The Z-score function is used to merge the citation lines. The colored connection curves originating from the citation map and pointing to the cited map show the context of the citations, called citation paths. As shown in Figure 9, there are mainly 3 citation paths: The green citation line indicates that research from medical and clinical journals is often cited by molecular, biological, and genetic journals. The two orange citation lines indicate that research from molecular, biological, and immunological journals is often cited by molecular, biological, genetic, nursing, and medical journals. In summary, the dual-map overlay analysis reveals the disciplinary connections and knowledge flows between different academic journals in this research field.

Figure 9 Clustering relationship of journal analysis.

Discussion

MF is a reactive remodeling process in response to myocardial injury, mainly manifested by the proliferation of myocardial fibroblasts and the excessive production and deposition of ECM proteins to replace the damaged tissue. However, the excessive generation and deposition of ECM, along with the increased ratio of type I and III collagen, lead to pathological fibrotic remodeling, which promotes the development of cardiac dysfunction and ultimately progresses to HF. This study applied CiteSpace 6.3.R2 and VOSviewer 1.6.20 literature analysis software to analyze the research hotspots and trends of oxidative stress in the field of MF from aspects of publication volume, authors, countries, institutional collaboration networks, as well as keyword co-occurrence, clustering, and burst words.

Publications on Oxidative Stress in MF

The overall publication volume of literature on oxidative stress-related MF has shown an upward trend, indicating that the research on oxidative stress in the field of MF is receiving increasing attention. It is predicted that the research hotspot will continue to increase, and the publication output is expected to maintain a growth trend in the coming years.

China ranks first in the world in terms of publication volume in the field of oxidative stress-related MF research. The intertwined and complex co-occurrence network map suggests that preliminary collaborative relationships have been established among institutions in different countries, but the in-depth cooperation between countries is currently mainly limited to some economically and technologically more developed nations. This indicates that although preliminary cooperation exists, international collaborative research still needs to be strengthened. It is recommended to establish national academic exchange programs to promote exchange and cooperation among different institutions internationally, which can leverage complementary strengths to produce more fruitful research results and provide more effective methods for the prevention and treatment of MF.

The publishing institutions are mainly concentrated in medical universities and some comprehensive universities, with Shandong University having the highest publication volume. However, there is not yet a globally comprehensive collaborative network among different institutions, which is not conducive to the long-term stable development of this field. Therefore, we suggest that research institutions in different countries should carry out more comprehensive and in-depth collaborative research to promote the development of the global research network on oxidative stress in MF.

In terms of the authors, Sowers, James R, Habibi, Javad, Nagata, Kohzo, and Young, Morag J have had a significant impact in this field, and following the achievements of these authors will help better understand the frontier dynamics and development trends in this field.

Most of the research on oxidative stress in MF is published in the journal “International Journal of Molecular Sciences” (n = 42), which has an impact factor of 4.9, is in the Q1 quartile, and publishes articles related to biochemistry, molecular and cellular biology, molecular biophysics, and molecular medicine, among others. In addition, the overlaid journal map (Figure 9) shows that “medicine, clinical, molecular” is frequently cited in “molecular, biology, genetics”, indicating that the current research on oxidative stress in the field of MF is increasingly focused on basic research.

Mechanisms of Oxidative Stress in MF

①Cell Injury and Cell Death: Oxidative stress can lead to excessive production of ROS, which can directly damage the DNA, proteins, and lipids of cardiomyocytes, causing impaired cell function. Persistent oxidative stress can also trigger cell apoptosis pathways, leading to cardiomyocyte death, which is one of the important causes of MF.②Activation of Signaling Pathways: ROS can act as signaling molecules, activating multiple signaling pathways related to fibrosis. ROS can activate the TGF-β signaling pathway, inducing the proliferation and differentiation of CFs into myofibroblasts, which then secrete large amounts of collagen and other ECM components, leading to MF.¹⁸ Empagliflozin can inhibit oxidative stress and fibrosis by suppressing the TGF-β/Smad pathway and activating the Nrf2/ARE signaling transduction.¹⁹ ROS can also promote CF proliferation and accelerate the development of MF by activating the MAPK-ERK/JNK pathway.²⁰ ③Mitochondrial Dysfunction: Oxidative stress can damage mitochondria, leading to mitochondrial dysfunction. Mitochondria are the “power plants” of the cell, and their impaired function can further exacerbate the energy metabolism disorder of cardiomyocytes, thereby promoting the occurrence of fibrosis. Related studies have shown that 2-APQC, a SIRT3 activator, can alleviate myocardial hypertrophy and fibrosis by regulating mitochondrial homeostasis, which may provide a new clue for the development of future heart failure treatments.²¹ ④Aggravation of Inflammatory Response: Oxidative stress can activate signaling pathways such as nuclear factor-κB (NF-κB), thereby upregulating the expression of various inflammatory factors, such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). These inflammatory factors not only exacerbate the injury to cardiomyocytes but also promote the activation and proliferation of fibroblasts, accelerating the progression of MF.^22,23 ⑤Regulation of Matrix Metalloproteinases (MMPs): MMPs can participate in the degradation and deposition of collagen in the myocardial interstitium, and tissue inhibitors of metalloproteinases (TIMPs) can inhibit the activity of MMPs. The TIMPs/MMPs system is the main target for maintaining the dynamic balance between collagen synthesis and metabolism, playing a role in maintaining the normal structure and function of the myocardium.²⁴ ROS can activate MMPs, inducing cardiomyocyte hypertrophy, apoptosis, and interstitial fibrosis,²⁵ thereby promoting the formation of MF.

Research Focus Evolution of Oxidative Stress Related Studies in MF

Based on the analysis of keyword co-occurrence networks and clustering, this paper summarizes the evolving research focuses on the role of oxidative stress in MF, which mainly includes the following aspects:

Activation of the Renin-Angiotensin-Aldosterone (RAAS) System

The widespread activation of the RAAS system accompanies the entire process of the occurrence and development of MF, which can promote oxidative stress and lead to cardiac hypertrophy, fibrosis, arterial stiffness, and inflammatory response.²⁶ Angiotensin II (Ang II) mediates multiple effects, including cell proliferation, migration, and ECM protein synthesis, through its Angiotensin II Type 1 Receptor (AT1R) in CFs.²⁷ Wang et al²⁸ confirmed that Ang II activates AT1R to induce the expression of transforming growth factor-β (TGF-β), promoting the activation of CFs and stimulating collagen synthesis and deposition. Ang II can also promote CFs to secrete interleukin-6, which upregulates TGF-β and phosphorylates Smad3 protein, thereby promoting MF.²⁹ Aldosterone can directly induce inflammation and oxidative stress responses by activating NADPH oxidase and mitochondria to generate reactive oxygen species, upregulating TGF-β, and promoting the development of MF.³⁰ Angiotensin-converting enzyme inhibitors (ACEIs), Angiotensin II Type 1 Receptor blockers (ARBs), and mineralocorticoid receptor antagonists (MRAs) have been proven to reduce the occurrence of MF, induce cardiac reverse remodeling, and alleviate cardiac diastolic dysfunction.^31–34

Mechanisms Regulating Oxidative Stress in MF Due to Different Etiologies

According to the etiology and anatomy, MF can be divided into reactive interstitial fibrosis and replacement fibrosis.³⁵ Diffuse fibrosis refers to the increased deposition of ECM caused by increased myocardial pressure load, with diffuse deposition of fibrous tissue in the interstitium and around blood vessels, which is often found in non-ischemic cardiomyopathy, valvular heart disease, and normal aging of the heart.^36,37 The release of inflammatory cytokines and chemokines, as well as changes in cell signaling caused by persistent oxidative stress, may promote the MF process.³⁸ Replacement fibrosis is more common after acute myocardial infarction (AMI) and hypertrophic cardiomyopathy, forming localized fibrotic scars in the infarcted myocardium, which are mainly composed of type I collagen. This type of fibrosis is part of the repair process and helps maintain the integrity of the ventricular structure and prevent ventricular wall rupture.^39,40 During the cardiac repair process, excessive ROS are produced, which promote the transformation of CFs into myofibroblasts and increase the deposition of ECM.^41,42

Understanding the different types of MF is crucial for developing appropriate treatment strategies and improving patient prognosis. Treatment strategies should be customized based on the specific nature and exact timing of the adverse myocardial remodeling events.

New Advances in Controlling Oxidative Stress as a Strategy Against MF

① CAR-T cell therapy: CAR T cells can target specific fibrosis-related proteins to reduce fibrosis.⁴³ The team led by Joel G. Rurik1 used modified messenger RNA (mRNA) to deliver CAR to mouse T cells, reprogramming T cells in vivo to reverse MF and restore cardiac function in HF mice.⁴⁴ ② Gene regulation: Bromodomain and extraterminal (BET) proteins are a highly conserved and widely expressed acetyl-lysine reading protein family that can collectively activate transcription. Their small molecule inhibitors have become an effective tool for reversibly interfering with the signaling transduction from enhancers to promoters in vivo.⁴⁵ Systemic administration of BET inhibitors can improve HF in mice.⁴⁶ BET inhibitors may regulate MF through the transcription factor MEOX1 in CFs, as the MEOX1-dependent transcriptional switch can control the state of CFs in HF, making MEOX1 a potential new therapeutic target for MF.⁴⁷③ Exosome therapy from different stem cell sources: Exosomes are 30–200 nm extracellular vesicles secreted by various cell types, carrying specific proteins, lipids, nucleic acids, and glycoconjugates, and participating in intercellular communication.⁴⁸ Studies have shown that exosomes from different stem cell sources can significantly reduce or inhibit MF in vivo and in vitro during pathological pro-fibrotic changes in the myocardium, replacing stem cell-based cardiac repair.⁴⁹ This therapy regulates the pathological formation of MF by transmitting information through internal miRNAs and regulating target cells, and has the potential to guide disease diagnosis and treatment. ④ Gut microbiota and their metabolites: Based on the gut microbiota and their metabolites, multiple new strategies for the treatment and prevention of MF have emerged, including dietary interventions, antibiotics, probiotics, and fecal microbiota transplantation.⁵⁰ These methods influence the progress of MF by regulating the systemic and local inflammatory response and oxidative stress of the host.^51,52

Trends in Oxidative Stress in MF-Related Research

The NLRP3 inflammasome is a multi-protein complex composed of the nucleotide-binding oligomerization domain-like receptor (NLR) family member NLRP3, the adaptor protein apoptosis-associated speck-like protein (ASC), and the effector caspase-1 (caspase-1).⁵³ The NLRP3 inflammasome is expressed at a low basal level in the healthy heart to maintain the structural integrity of the cardiac ECM. In the early stage of the post-AMI response, the NLRP3 inflammasome is activated in the inflammatory response secondary to myocardial injury, which can promote wound healing, tissue repair, and induce myofibroblast formation after AMI.⁵⁴ In diabetic cardiomyopathy, the NLRP3 inflammasome induces an increase in TGF-β and IL-1β, activating the pro-fibrotic mediators TGF-β receptor, AT1R, and IL-1R in the myocardium to induce ROS generation and promote myofibroblast formation.⁵⁵ The mechanism by which the NLRP3 inflammasome expression leads to myofibroblast formation is complex, involving multiple pathways, including the TGF/Smads signaling pathway,⁵⁶ the TLR-4/NF-κβ signaling pathway,⁵⁷ and the cGMP-PKG signaling pathway,⁵⁸ but the specific intracellular signaling pathways and biological mechanisms are still unclear. Potential therapeutic strategies targeting the NLRP3 inflammasome may help alleviate myofibroblast formation and improve cardiac function, providing a direction for the development of new treatments. Some potential therapeutic strategies are under investigation, such as NLRP3 inhibitors that have shown inhibitory effects on NLRP3 activity in various animal models,^59–61 and IL-1β receptor antagonists that can indirectly inhibit its inflammatory effects,^62–64 although they have not yet been applied to myofibroblast-related diseases and require further basic and clinical studies to verify their safety and efficacy. Recent studies have demonstrated that certain pharmacological agents can modulate the NLRP3 inflammasome and its upstream and downstream targets. However, the mechanisms linking different pathways and their resultant effects remain unclear, necessitating further investigation into the hierarchical relationships between these pathways. Future research should focus on extensive docking studies between various compounds and targets to identify drugs that can sustainably and efficiently inhibit NLRP3 inflammasome activation. Additionally, elucidating the precise mechanisms of action will be crucial for mitigating MF and improving cardiac dysfunction.

In summary, based on bibliometric analysis, this study summarized the current status, evolutionary process, and latest progress of oxidative stress research in the field of myofibroblasts from the establishment of the database to December 31, 2024, and analyzed its prospects and development trends. Currently, the study of oxidative stress in myofibroblast-related diseases is in a period of rapid development. The pathological mechanism of myofibroblast formation is complex, and we need to conduct more in-depth research on the oxidative stress-related mechanisms of myofibroblast formation from the perspective of precision treatment, in order to develop new drugs, explore new therapeutic targets and strategies, and provide more options for the prevention and treatment of myofibroblast-related diseases. The activation of the NLRP3 inflammasome signaling pathway by oxidative stress to promote myofibroblast formation may be a future research trend and deserves further exploration and study.