Journal of Inflammation Research

Mitochondria and Inflammation Crosstalk in Human Disease: Immunometabolism, Cell Death, and Therapeutic Targets

The Journal of Inflammation Research is pleased to welcome you to submit your research to the Article Collection "Mitochondria and Inflammation Crosstalk in Human Disease: Immunometabolism, Cell Death, and Therapeutic Targets".

Mitochondria help coordinate inflammatory responses through energy metabolism, redox signaling, and the release of molecules that activate innate immune sensors. Inflammatory signals can, in turn, alter mitochondrial function, creating feedback between cellular stress and immune activation. This Article Collection will examine how that relationship contributes to human disease, with particular attention to immune metabolism and regulated cell death. We seek work that explains when mitochondrial responses support host defense and tissue repair, when they sustain harmful inflammation, and how these outcomes depend on cell type, disease stage, and the tissue environment.

Understanding these distinctions is essential for developing treatments that limit tissue injury while preserving protective immunity. Changes in mitochondrial respiration, metabolite availability, and quality control may influence inflammatory signaling, but their functional significance requires careful testing. The Collection will bring together mechanistic studies and investigations in patient samples or clinically relevant models to connect mitochondrial alterations with inflammatory outcomes. It will address infectious and sterile inflammation across cardiovascular, metabolic, autoimmune, and neurodegenerative diseases, as well as aging. Contributions should explain what their findings establish about disease mechanisms and, where relevant, the evidence supporting therapeutic intervention.

We welcome original research and review articles on mitochondrial DNA and RNA sensing; cGAS–STING and inflammasome signaling; reactive oxygen species and lipid peroxidation; succinate, itaconate, and other immunoregulatory metabolites; mitochondrial dynamics, mitophagy, and organelle communication; and the relationship of apoptosis, pyroptosis, necroptosis, and ferroptosis to inflammation. Studies using human immune cells, patient-derived induced pluripotent stem cells, organoids, or tissue models are encouraged, alongside informative animal studies. Single-cell, spatial, and other omics approaches are welcome when they address a defined inflammatory question, particularly with functional validation. Therapeutic studies may examine mitochondrial quality control, metabolic enzymes, redox pathways, or innate immune sensors, with attention to target engagement, selectivity, and effects on host defence.

Keywords: Mitochondrial dysfunction; Inflammation; Immunometabolism; Regulated cell death; Therapeutic targets

Meet the Guest Advisors

Dr. Ankit Kushwaha is a Postdoctoral Scholar in Pediatric Cardiology at Stanford University School of Medicine. His research investigates mitochondrial and endothelial dysfunction in congenital heart disease using patient-derived induced pluripotent stem cell models, molecular profiling, and drug screening. He received his PhD in Biotechnology from Motilal Nehru National Institute of Technology Allahabad, where he studied how bacterial quorum-sensing molecules affect organelle stress, autophagy, apoptosis, and inflammation in human macrophages. His research interests center on connecting cellular stress mechanisms with therapeutic opportunities in human disease.

Professor Vishnu Agarwal is a Professor in the Department of Biotechnology at Motilal Nehru National Institute of Technology Allahabad, India. His research focuses on infection biology, and immunomodulation by drugs and herbal formulations. His work includes studies of how microbial signaling molecules alter calcium signaling, mitochondrial function, autophagy, and cell death in immune cells. His research connects host-pathogen interactions with inflammatory mechanisms and approaches to therapeutic intervention.