We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
A potential therapeutic approach for ulcerative colitis: targeted regulation of mitochondrial dynamics and mitophagy through phytochemicals
Summary
This review explored how plant-based compounds could be used to treat ulcerative colitis by targeting mitochondrial function. Researchers discussed how dysfunctional mitochondria generate excessive reactive oxygen species that drive intestinal inflammation. While focused on therapeutic approaches rather than microplastics directly, the study is relevant to understanding how environmental stressors that damage mitochondria may contribute to gut inflammation.
Mitochondria are important organelles that regulate cellular energy and biosynthesis, as well as maintain the body's response to environmental stress. Their dynamics and autophagy influence occurrence of cellular function, particularly under stressful conditions. They can generate reactive oxygen species (ROS) which is a major contributor to inflammatory diseases such as ulcerative colitis (UC). In this review, we discuss the key effects of mitochondrial dynamics and mitophagy on the pathogenesis of UC, with a particular focus on the cellular energy metabolism, oxidative stress, apoptosis, and immunoinflammatory activities. The therapeutic efficacy of existing drugs and phytochemicals targeting the mitochondrial pathway are discussed to reveal important insights for developing therapeutic strategies for treating UC. In addition, new molecular checkpoints with therapeutic potential are identified. We show that the integration of mitochondrial biology with the clinical aspects of UC may generate ideas for enhancing the clinical management of UC.
Sign in to start a discussion.
More Papers Like This
Role of Mitochondria in Inflammatory Bowel Diseases: A Systematic Review
This systematic review found that mitochondrial dysfunction plays a significant role in inflammatory bowel diseases through multiple mechanisms, including disrupted energy production, impaired mucosal repair, altered gut microbiota signaling, and weakened intestinal barrier integrity. The findings are relevant to microplastic research because plastic particle exposure has been shown to cause mitochondrial damage in gut tissues.
Mitochondria-Targeted Biomaterials-Regulating Macrophage Polarization Opens New Perspectives for Disease Treatment
This review explores how new biomaterials can be designed to target mitochondria inside immune cells called macrophages, steering them between pro-inflammatory and anti-inflammatory states to treat diseases. While not directly about microplastics, the review is relevant because microplastic exposure is known to cause mitochondrial damage and trigger inflammatory immune responses through these same pathways. Understanding how to control macrophage behavior through mitochondria could lead to treatments for inflammation caused by environmental pollutants like microplastics.
The Mitochondrial Battleground: A Review of Microplastic-Induced Oxidative Stress and Inflammatory Pathways in Human Health
This review synthesizes research on how microplastics damage mitochondria through oxidative stress and inflammation across aquatic, terrestrial, and mammalian systems. Researchers found that microplastics generate reactive oxygen species that disrupt mitochondrial function, with smaller and aged particles causing greater toxicity, while inflammatory signaling creates a feedback loop that worsens cellular damage.
Hypoxia is a key mechanism for regulating inflammation in ulcerative colitis
This review examines how tissue hypoxia regulates inflammation in ulcerative colitis, a chronic bowel disease. While not directly about microplastics, it is relevant because microplastic exposure has been associated with gut inflammation and disruption of the intestinal barrier in emerging research.
Assessing micro and nanoplastics toxicity using rodent models: Investigating potential mitochondrial implications
This review examines recent rodent studies investigating how micro- and nanoplastics affect cellular health, with a focus on potential mitochondrial impacts. Researchers found that while no study has directly targeted mitochondrial effects, several reported molecular and biochemical changes consistent with disrupted mitochondrial function, including oxidative stress. The study suggests that mitochondria may be an important but understudied target of micro- and nanoplastic toxicity.