Autophagy plays an important role in the renewal of cellular components, which function in energy production, metabolism, and clearance of damaged organelles. Both macroautophagy and microautophagy are involved in these processes. Although it was thought that nonselective macroautophagy is responsible for the clearance of damaged or old organelles, recent studies show that the clearance of cellular organelles depends on selective processes. Mitophagy is a process for selective degradation of mitochondria, which is well documented. The selective autophagy for other organelles includes endoplasmic reticulum autophagy (reticulophagy) and peroxisome autophagy (pexophagy). Autophagy is a routine pathway for cells to degrade unused proteins and damaged organelles in cells. Autophagy selectively removes dysfunctional cellular components but not damages the normally functioning organelles, to maintain the homeostasis of cells. In addition to the maintenance of the homeostasis of cells, autophagy clears the damaged organelles in disease or injury conditions to achieve cellular quality control. In some differentiated cells, such as red blood cells, some organelles are removed during the maturation, including mitochondria. The autophagy system can selectively clear the mitochondria and other organelles, which lead to the maturation of red blood cells. Dysfunction of autophagy impairs the clearance of damaged organelles, which results in injury of cells. In the maturation of red blood cells, failure to clear the cellular organelles by autophagy will disturb the normal differentiation of red blood cells, leading to a series of diseases such as anemia.
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Tokyo Metropolitan Inst Med Sci, Dept Bioregulat & Metab, Tokyo 1138613, JapanTokyo Metropolitan Inst Med Sci, Dept Bioregulat & Metab, Tokyo 1138613, Japan
Mizushima, Noboru
Hara, Taichi
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SORST, Japan Sci & Technol Agcy, Kawaguchi, JapanTokyo Metropolitan Inst Med Sci, Dept Bioregulat & Metab, Tokyo 1138613, Japan
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Columbia Univ, Dept Med, New York, NY 10032 USAColumbia Univ, Dept Med, New York, NY 10032 USA
Huebener, Peter
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Gwak, Geum-Youn
Pradere, Jean-Philippe
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Columbia Univ, Dept Med, New York, NY 10032 USAColumbia Univ, Dept Med, New York, NY 10032 USA
Pradere, Jean-Philippe
Quinzii, Catarina M.
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Columbia Univ, Dept Neurol, New York, NY 10032 USAColumbia Univ, Dept Med, New York, NY 10032 USA
Quinzii, Catarina M.
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Friedman, Richard
Lin, Chyuan-Sheng
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Columbia Univ, Dept Pathol & Cell Biol, New York, NY 10032 USAColumbia Univ, Dept Med, New York, NY 10032 USA
Lin, Chyuan-Sheng
Trent, Chad M.
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Columbia Univ, Dept Med, Div Prevent Med & Nutr, New York, NY 10032 USA
Columbia Univ, Inst Human Nutr, New York, NY 10032 USAColumbia Univ, Dept Med, New York, NY 10032 USA
Trent, Chad M.
Mederacke, Ingmar
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Columbia Univ, Dept Med, New York, NY 10032 USAColumbia Univ, Dept Med, New York, NY 10032 USA
Mederacke, Ingmar
Zhao, Enpeng
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Albert Einstein Coll Med, Marion Bessin Liver Res Ctr, Dept Med, Bronx, NY 10461 USAColumbia Univ, Dept Med, New York, NY 10032 USA
Zhao, Enpeng
Dapito, Dianne H.
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Columbia Univ, Inst Human Nutr, New York, NY 10032 USAColumbia Univ, Dept Med, New York, NY 10032 USA
Dapito, Dianne H.
Lin, Yuxi
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Columbia Univ, Inst Human Nutr, New York, NY 10032 USAColumbia Univ, Dept Med, New York, NY 10032 USA
Lin, Yuxi
Goldberg, Ira J.
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Columbia Univ, Dept Med, Div Prevent Med & Nutr, New York, NY 10032 USA
Columbia Univ, Inst Human Nutr, New York, NY 10032 USAColumbia Univ, Dept Med, New York, NY 10032 USA
Goldberg, Ira J.
Czaja, Mark J.
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Albert Einstein Coll Med, Marion Bessin Liver Res Ctr, Dept Med, Bronx, NY 10461 USAColumbia Univ, Dept Med, New York, NY 10032 USA
Czaja, Mark J.
Schwabe, Robert F.
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Columbia Univ, Dept Med, New York, NY 10032 USA
Columbia Univ, Inst Human Nutr, New York, NY 10032 USAColumbia Univ, Dept Med, New York, NY 10032 USA