Apoptosis

Overview

Apoptosis is a tightly regulated form of programmed cell death by which organisms eliminate superfluous, damaged, or potentially dangerous cells while preserving tissue integrity. It proceeds through orderly morphological and biochemical events, including chromatin condensation, cell shrinkage, membrane blebbing, and fragmentation into apoptotic bodies that are cleared without inflammation. Two principal pathways converge on the activation of caspases: the intrinsic mitochondrial pathway, governed by the balance of pro- and anti-apoptotic BCL-2 family proteins such as BCL-2 and BAK and the release of cytochrome c, and the extrinsic pathway triggered by death-receptor ligation. Apoptosis maintains hematopoietic homeostasis, shapes immune-cell repertoires, and removes mutated cells, and its dysregulation is a hallmark of disease. In oncology, evasion of apoptosis permits malignant survival and contributes to therapeutic resistance, while many cytotoxic and targeted agents act by restoring apoptotic signaling; acquired resistance to apoptosis induction is a recognized obstacle in cancer cells. Apoptotic processes also intersect with metabolic stress, oxidative injury, and the biology of stored blood components. The journal publishes peer-reviewed research on apoptotic regulation and its molecular machinery, including BCL-2 family signaling, resistance mechanisms in malignancy, metabolic and oxidative modulation of cell death, and the therapeutic targeting of apoptosis in cancer and related conditions.

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 82 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
• CGRP expression and signaling sensitization in a mouse model of chronic oxaliplatin-induced peripheral neuropathy
  2026 · Molecular Pain
• 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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