We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Targeting Regulated Cell Death Pathways in COPD: Mechanisms and Therapeutic Strategies
Summary
This review examines how multiple regulated cell death pathways — including apoptosis, necroptosis, pyroptosis, ferroptosis, and autophagy — contribute to chronic obstructive pulmonary disease progression and discusses these pathways as potential therapeutic targets.
Chronic obstructive pulmonary disease (COPD) is a progressive lung disease defined by persistent airflow limitation, chronic inflammation, and ongoing airway remodeling, and poses a substantial global health challenge. Despite its clinical significance, the underlying cellular mechanisms remain poorly defined. Regulated cell death (RCD) incorporates various kinds of cell death that are typically regulated by specific molecular pathways. Numerous new kinds of RCD have been identified outside of the traditional apoptotic pathway, like necroptosis, pyroptosis, ferroptosis, autophagy, cuproptosis, and parthanatos. To date, there is growing evidence indicating that these pathways participate in the regulation of COPD development. However, their specific roles and therapeutic relevance remain poorly understood. In this review, we discuss a summary of the molecular mechanisms by which RCD pathways influence the onset and advancement of COPD. Additionally, the therapeutic benefits of agents that target these cell death pathways in COPD treatment were described. By integrating current insights, this review aims to broaden our knowledge of the pathophysiology of COPD and offer novel approaches to treatment.
Sign in to start a discussion.
More Papers Like This
The interplay of ferroptosis and oxidative stress in pulmonary fibrosis: from mechanisms to treatment
This research review summarizes how a specific type of cell death called ferroptosis may contribute to pulmonary fibrosis, a serious lung disease where scar tissue builds up and makes breathing difficult. Scientists have found that when cells die from iron buildup and damage from harmful molecules, it can worsen lung scarring, but drugs that block this process show promise in animal studies. Understanding this connection could lead to new treatments for people with pulmonary fibrosis, though more research is needed to make sure these potential medicines are safe and effective in humans.
Advances in the regulatory mechanisms of mTOR in necroptosis
This review explores how the mTOR signaling pathway regulates necroptosis, a form of programmed cell death distinct from apoptosis. Researchers describe multiple mechanisms through which mTOR influences cell death, including direct regulation of key necroptosis proteins, indirect effects through autophagy, and modulation of reactive oxygen species. The study highlights that mTOR can both promote and inhibit necroptosis depending on the context, making it a complex but promising therapeutic target.
Mitochondrial dysfunction–induced PANoptosis: Mechanisms, triggers, and disease implications
This review provides a comprehensive overview of PANoptosis, a recently identified form of cell death that combines features of three previously distinct pathways: pyroptosis, apoptosis, and necroptosis. Researchers describe how mitochondrial dysfunction can trigger this integrated cell death response, with implications for infections, inflammation, cancer, and degenerative diseases. The study highlights PANoptosis as an important emerging concept for understanding how cells respond to environmental and biological stressors.
Microplastics exacerbate ferroptosis via mitochondrial reactive oxygen species-mediated autophagy in chronic obstructive pulmonary disease
Researchers found that microplastics worsen chronic obstructive pulmonary disease (COPD) by triggering a chain reaction in lung cells: the plastics damage mitochondria (the cell's energy centers), which produces harmful molecules that activate a self-destructive process called autophagy-dependent ferroptosis. Lung tissue from COPD patients contained significantly higher concentrations of polystyrene microplastics than healthy controls. When scientists blocked this destructive pathway in mice, it reduced the excessive inflammation and prevented COPD flare-ups caused by microplastic exposure.
Bibliometric analysis of global research trends on pyroptosis in lung disease
This bibliometric analysis mapped global research trends on pyroptosis (inflammatory cell death) in lung disease from 2000 to the present, identifying key countries, institutions, and collaboration networks driving this emerging field. The analysis shows growing research attention on the link between pyroptosis and acute lung injury, with future focus likely to expand to other lung conditions.