Apoptosis

Overview

Apoptosis is a tightly regulated form of programmed cell death essential for development, tissue homeostasis, and the elimination of damaged or potentially dangerous cells. It proceeds through intrinsic (mitochondrial) and extrinsic (death-receptor) pathways that converge on caspase activation, producing characteristic features such as chromatin condensation, DNA fragmentation, membrane blebbing, and formation of apoptotic bodies. Regulation by the BCL-2 family and other factors balances pro- and anti-apoptotic signals; dysregulation contributes to cancer, neurodegeneration, and other disease, making apoptotic pathways important therapeutic targets. Research grouped under this topic examines apoptosis across cellular, oncological, and toxicological contexts. Studies investigate the relationship between glucose levels and apoptosis in stored platelets, resistance to butyrate-induced apoptosis in colorectal cancer cells through gene-expression analysis, and the role of BCL-2 and BAK genes in chronic kidney disease and hemodialysis patients. Additional work addresses oxidative stress and apoptosis in testicular tissue, prostate apoptosis response protein-4 and its effect on metastasis, cytotoxic and apoptotic activity of silver nanoparticles on cancer cell lines, and complementary approaches to cancer prevention. Studies on neuronal cell damage and liposome photoactivity further situate apoptosis within cell-injury and delivery research. This peer-reviewed literature supports researchers investigating cell-death mechanisms, their dysregulation in disease, and apoptosis-targeted therapeutic strategies.

Research published in this journal

12 peer-reviewed articles, ranked by relevance. Each links to its DOI.

How this research is being cited

The 12 articles above have been cited 85 times in the scholarly literature. Citation data via OpenAlex and Crossref, updated Jun 2026.

• High-Intensity Interval and Aerobic Training Alleviate Cardiac Pathology, Apoptosis, and Atrial Fibrillation in Rats with Chronic Kidney Disease: The Roles of FGF23 and Klotho
  2026 · Biomolecules
• Zn glycine attenuates LPS-induced inflammatory bone loss in geese through suppression of osteoclastogenesis via reducing TLR-4/NFκB signaling
  2026 · Ecotoxicology and Environmental Safety
• Nephroprotective Effect of L-Carvone on a Mouse Model of LPS-Induced Sepsis-Associated Renal Injury via Regulation of TLR4/NF-κB/AP-1/IRF-3 and Nrf2/iNOS Molecular Signaling Cascades
  2026 · Journal of Taibah University Medical Sciences
• L-carvone alleviates lipopolysaccharide-Induced acute kidney injury via modulating MyD88-dependent and independent signaling pathways in Mice
  2026 · Molecular Biology Reports
• Fraisinib in a Shell: Liposomal Encapsulation of a GARS1 Inhibitor for Controlled Anticancer Delivery
  2026 · AAPS PharmSciTech
• Monosodium glutamate exacerbated the lipopolysaccharide-induced reproductive toxicity of male Wistar rats
  2025 · BMC Pharmacology and Toxicology
• Atrazine alters nitric oxide secretion and cytokines production in LPS-stimulated BalB/c mice, RAW264.7 macrophage and THP-1 cell lines
  2025 · Chemosphere
• Meprin β regulates osteopontin-signaling in ischemia/reperfusion-induced kidney injury
  2025 · BMC Nephrology

A sample of recent works citing this journal's research on Apoptosis, linking to each citing work.

This page summarises published research for orientation; it is not medical or professional advice.

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