Impact of mitochondrial damage on tumor microenvironment and immune response: a comprehensive bibliometric analysis

Abstract

Background: Mitochondrial damage contributes to apoptosis, oxidative stress, and inflammation, which collectively impact the immune system's function and the tumor microenvironment (TME). These processes, in turn, influence tumor cell growth, migration, and response to treatment.

Objective: We conducted a bibliometric analysis to elucidate the complex interactions between mitochondrial damage, the immune system, and the TME.

Methods: Data were sourced from the Science Citation Index Core Collection (WoSCC) and analyzed using advanced tools like VOSviewer and Citespace. Our focus was on literature published between 1999 and 2023 concerning the interactions between mitochondrial damage and the TME, as well as immune responses to tumors. The analysis included regional contributions, journal influence, institutional collaborations, authorship, co-cited authors, and keyword citation bursts.

Results: Our research encompassed 2,039 publications, revealing an increasing trend in annual output exploring the relationship between mitochondrial damage, TME dynamics, and immune responses. China, the United States, and South Korea emerged as the leading contributors. Prominent institutions included Institut National de la Santé et de la Recherche Médicale, University of Texas System, China Medical University, and Sun Yat-sen University. Key journals in this field are the International Journal of Molecular Sciences, Mitochondrion, and the European Journal of Pharmacology. Liang H and Wallace DC were identified as the most productive and co-cited authors, respectively. Keyword analysis highlighted the critical roles of inflammatory responses, oxidative stress, and the immune system in recent research.

Conclusion: This bibliometric analysis provides a comprehensive overview of historical and current research trends, underscoring the pivotal role of mitochondrial damage in the TME and immune system.

Keywords: bibliometric analysis; immune response; mitochondrial damage; oxidative stress; tumor microenvironment.

Figure 1

Flowchart detailing the inclusion process of studies for the bibliometric analysis.

Figure 2

Annual publication and citation trends on mitochondrial dysfunction in the TME from 1999 to 2023. The left vertical axis indicates the annual publication count, while the right vertical axis represents the annual citation frequency. Blue dots represent the number of articles published each year, and the light black curve depicts the citation frequency over the same period.

Figure 3

Visualization of annual publication trends and international collaborations from 1999 to 2023. (A) Annual publication trends for the top 10 contributing countries/regions. (B) Countries/regions collaboration network. Each node represents a country or region, with node size indicating their publication volume. Nodes of the same colour belong to the same category.

Figure 4

Inter-institutional collaboration network. Each node represents an institution, with node size proportional to the volume of publications contributed to the field of mitochondrial dysfunction in the TME. Lines between institutions represent collaborative relationships.

Figure 5

Journal collaboration network. Each node in this network diagram represents a scientific journal. Node size is proportional to the volume of publications contributed by that journal to the field of mitochondrial dysfunction in the TME. Lines connecting the nodes illustrate collaborations between journals, with thicker lines indicating more frequent cross-citations or shared authorship.

Figure 6

Analysis of authors and co-cited authors. (A) Visualization map of author analysis. (B) Visualization map of co-cited author analysis. Each node represents an author or co-cited author, with node size indicating their citation count or document volume. Lines between authors represent collaborative relationships.

Figure 7

Keyword visualization and analysis. (A) Network visualization of keywords using VOSviewer, where node sizes increase with keyword frequency. (B) The 25 most frequently cited keywords relevant to mitochondrial dysfunction in the TME. The term “strength” refers to the connection intensity between two nodes, as determined by the software.

Figure 8

Interactions between mitochondrial damage, the immune system, the tumor microenvironment (TME), and cancer treatments. This diagram illustrates how mitochondrial damage influences CD8+ T cells and macrophages, leading to increased reactive oxygen species (ROS) production, cell cycle arrest, and apoptosis in tumor cells. Cancer treatments such as photodynamic therapy, nanomedicine, and immunotherapy target these interactions to enhance antitumor responses and inhibit tumor growth. The diagram underscores the critical role of mitochondrial damage in modulating immune responses and tumor progression, offering insights for improved cancer therapies.