ReviewInternational journal of molecular sciences2026
Autophagy Defects and Mitochondrial Retention in Erythroid Diseases.
Review in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
9 authors.
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Abstract
Erythropoiesis requires extensive cellular remodeling, culminating in enucleation and organelle clearance to generate mature red blood cells (RBCs). Over the past 15 years, accumulating evidence has established that macroautophagy-particularly ULK1-, NIX-, and PINK1-dependent mitophagy-plays a central role in erythroid maturation. Defective autophagy can lead to mitochondrial retention, increased reactive oxygen species (ROS) production, membrane alterations, and ineffective erythropoiesis. Such abnormalities have now been documented in several hematological disorders, including myelodysplastic syndromes, Fanconi anemia, Diamond-Blackfan anemia, sickle cell disease, and β-thalassemia. This review summarizes current knowledge of autophagy regulation during erythropoiesis, the molecular mechanisms governing mitochondrial clearance, and the pathological consequences of impaired autophagy in red blood cell disorders. Finally, we discuss emerging therapeutic strategies targeting autophagy pathways.
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