Apoptosis

Overview

Apoptosis is a tightly regulated form of programmed cell death by which cells dismantle themselves in an orderly, non-inflammatory manner, characterized by chromatin condensation, DNA fragmentation, membrane blebbing, and formation of apoptotic bodies that are cleared by phagocytes. It proceeds through two principal routes: the intrinsic (mitochondrial) pathway, governed by the balance of pro- and anti-apoptotic BCL-2 family proteins such as BCL-2, BAK, and BAX that control mitochondrial outer membrane permeabilization and cytochrome c release; and the extrinsic pathway, triggered by death-receptor ligation at the cell surface. Both converge on the activation of caspases, the proteases that execute cellular demolition. Apoptosis is essential for development, tissue homeostasis, and elimination of damaged or potentially malignant cells, and its dysregulation contributes to cancer, neurodegeneration, and ischemic injury. Because evasion of apoptosis underlies tumor survival and drug resistance, inducing or restoring apoptotic signaling is a central therapeutic strategy. Research in this area examines apoptosis across varied experimental systems, including resistance mechanisms in colorectal and colon cancer cells, apoptosis-related gene expression in chronic kidney disease, oxidative stress-driven cell death in tissue, and the cytotoxic and pro-apoptotic activity of nanoparticles and candidate compounds. The journal publishes peer-reviewed research on the molecular regulation, pathological roles, and therapeutic modulation of apoptosis.

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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