Programmed Cell Death in Heart Failure: Mechanisms, Impacts, and Therapeutic Prospects
Dongda Wu1, Donghong Deng2, Biao Tang1,2
1Medical School, Hunan University of Chinese Medicine, 410208 Changsha, Hunan, China.
Insights
Programmed cell death (PCD) pathways are critical in heart failure. Targeting specific PCD mechanisms, like necroptosis and inflammation, shows promise for novel heart failure therapies.
Area of Science:
- Cardiology
- Cell Biology
- Pathophysiology
Background:
- Heart failure involves complex cellular death mechanisms.
- Programmed cell death (PCD) is a key factor in cardiac dysfunction.
- Understanding PCD is vital for treating heart failure.
Purpose of the Study:
- To review different forms of PCD in heart failure.
- To examine PCD mechanisms and therapeutic targets.
- To discuss novel therapeutic strategies for cardiac failure.
Main Methods:
- Literature review of recent research findings.
- Analysis of programmed cell death pathways (apoptosis, autophagy, necroptosis, pyroptosis, ferroptosis).
- Examination of therapeutic interventions targeting cell death and inflammation.
Main Results:
- PCD significantly contributes to heart failure progression.
- Inhibiting receptor-interacting protein kinases (RIPK1 and RIPK3) reduces cardiac injury.
- Targeting IL-1β may reduce both cell death and inflammation.
Conclusions:
- Programmed cell death is a pivotal factor in heart failure.
- Targeting specific PCD pathways offers promising therapeutic avenues.
- Novel strategies combining cell death and inflammation inhibition can improve heart failure management.
Abstract:
Heart failure is a complex pathological condition characterized by various mechanisms of cellular death, among which programmed cell death (PCD) plays a crucial role in the pathophysiology of cardiac dysfunction. This review delves into the different forms of PCD present in heart failure, including apoptosis, autophagy, necroptosis, pyroptosis, and ferroptosis, and examines the mechanisms of action involved and the potential therapeutic targets for treating cardiac failure. By analyzing the latest research findings, we reveal the pivotal role of PCD in the progression of heart failure and discuss the preclinical prospects of intervening in these processes to develop novel therapeutic strategies. For instance, pharmacological agents that inhibit receptor-interacting protein kinases (RIPK1 and RIPK3) involved in necroptosis have been demonstrated to reduce cardiac injury and improve functional outcomes. Additionally, targeting the inflammatory responses associated with necrotic cell death, such as using interleukin (IL)-1β inhibitors, may provide a dual benefit by reducing cell death and inflammation. Thus, combining current knowledge will enhance our understanding in this field and promote innovative approaches to managing heart failure more effectively.
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