Programmed cell death (PCD) is a fundamental biological process essential for organism growth, development, aging, and disease. It is a genetically controlled, autonomous, and orderly process involving the activation, expression, and regulation of a series of genes. Recent research has revealed new mechanisms of multiple PCD pathways. This review summarizes the various PCD pathways, analyzes their morphological characteristics and biomarkers, and discusses their roles in disease diagnosis and treatment, particularly in malignant tumors. PCD is divided into several types, including apoptosis, necroptosis, pyroptosis, ferroptosis, autophagy-dependent cell death, mitotic catastrophe, immunogenic cell death, entosis, parthanatos, cuproptosis, disulfidptosis, NETosis, lysosome-dependent cell death, alkaliptosis, and oxeiptosis. Each type has distinct morphological features, molecular mechanisms, and regulatory pathways. For example, apoptosis is characterized by nuclear condensation, cell membrane blistering, and the formation of apoptotic bodies. Necroptosis involves membrane rupture and inflammatory responses, while pyroptosis is associated with the release of inflammatory contents. Ferroptosis is caused by iron-dependent oxidative damage, and autophagy-dependent cell death involves the formation of autophagosomes. The molecular mechanisms of PCD are complex and involve various signaling pathways and regulatory systems. Apoptosis is regulated by intrinsic and extrinsic pathways, with the intrinsic pathway involving mitochondrial permeabilization and the extrinsic pathway involving death receptors. Necroptosis is regulated by a caspase-independent pathway, while pyroptosis is mediated by Gasdermin family proteins. Ferroptosis is characterized by lipid peroxidation and iron-dependent oxidative damage, and autophagy-dependent cell death involves the degradation of cellular components by lysosomes. Understanding the molecular mechanisms and regulatory pathways of PCD is crucial for developing targeted therapies for diseases, including cancer. Future research should focus on elucidating the molecular mechanisms of PCD, their interactions, and identifying specific drug targets. This knowledge can lead to more effective treatments for various diseases.Programmed cell death (PCD) is a fundamental biological process essential for organism growth, development, aging, and disease. It is a genetically controlled, autonomous, and orderly process involving the activation, expression, and regulation of a series of genes. Recent research has revealed new mechanisms of multiple PCD pathways. This review summarizes the various PCD pathways, analyzes their morphological characteristics and biomarkers, and discusses their roles in disease diagnosis and treatment, particularly in malignant tumors. PCD is divided into several types, including apoptosis, necroptosis, pyroptosis, ferroptosis, autophagy-dependent cell death, mitotic catastrophe, immunogenic cell death, entosis, parthanatos, cuproptosis, disulfidptosis, NETosis, lysosome-dependent cell death, alkaliptosis, and oxeiptosis. Each type has distinct morphological features, molecular mechanisms, and regulatory pathways. For example, apoptosis is characterized by nuclear condensation, cell membrane blistering, and the formation of apoptotic bodies. Necroptosis involves membrane rupture and inflammatory responses, while pyroptosis is associated with the release of inflammatory contents. Ferroptosis is caused by iron-dependent oxidative damage, and autophagy-dependent cell death involves the formation of autophagosomes. The molecular mechanisms of PCD are complex and involve various signaling pathways and regulatory systems. Apoptosis is regulated by intrinsic and extrinsic pathways, with the intrinsic pathway involving mitochondrial permeabilization and the extrinsic pathway involving death receptors. Necroptosis is regulated by a caspase-independent pathway, while pyroptosis is mediated by Gasdermin family proteins. Ferroptosis is characterized by lipid peroxidation and iron-dependent oxidative damage, and autophagy-dependent cell death involves the degradation of cellular components by lysosomes. Understanding the molecular mechanisms and regulatory pathways of PCD is crucial for developing targeted therapies for diseases, including cancer. Future research should focus on elucidating the molecular mechanisms of PCD, their interactions, and identifying specific drug targets. This knowledge can lead to more effective treatments for various diseases.