{"id":7076,"date":"2021-09-26T12:51:47","date_gmt":"2021-09-26T10:51:47","guid":{"rendered":"https:\/\/meddists.com\/learn\/pre-clinical\/pathology\/cell-injury-cell-death-and-adaptation\/adaptation\/atrophy-involution-and-apoptosis\/"},"modified":"2021-09-26T12:56:48","modified_gmt":"2021-09-26T10:56:48","slug":"atrophy-involution-and-apoptosis","status":"publish","type":"page","link":"https:\/\/meddists.com\/learn\/pre-clinical\/pathology\/cell-injury-cell-death-and-adaptation\/adaptation\/atrophy-involution-and-apoptosis\/","title":{"rendered":"Atrophy, Involution and apoptosis"},"content":{"rendered":"<span class=\"block-heading\" id=\"header_1\">\n<h2 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Atrophy<\/h2>\n<\/span><span class=\"block-content\" id=\"contents_1\">\n\n\n<p class=\"wp-block-paragraph\">An adaptive response characterized by decreased protein synthesis and increased protein degradation.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li><strong>Cells decrease in size<\/strong><\/li><li><strong>Degradation of proteins<\/strong> using:<ul><li>Lysosomes<\/li><li>Ubiquitin-proteasome pathway<\/li><\/ul><\/li><li><strong>Autophagy<\/strong><ul><li>&#8220;Self-eating&#8221;<\/li><li>Natural, regulated mechanism of the cell that disassembles unnecessary or dysfunctional components<\/li><li>Elimination of intracellular substances<\/li><li>Membrane-bound vacuoles containing mitochondria, ER, complex protein fragments and undegradable substances<ul><li>Undegradable substances accumulate, and with time, can be seen as <a href=\"https:\/\/meddists.com\/course\/pathology\/lessons\/pigments\/\">pigments<\/a> (lipofuscin and hemosiderin)<\/li><\/ul><\/li><li>Plays a role in many physiological and pathological processes<\/li><\/ul><\/li><li>Occurs due to:<ul><li>Decreased workload (inactivity)<\/li><li>Reduced blood supply or innervation<\/li><li>Nutritional defect (cachexia)<\/li><li>Loss of hormonal stimulation<\/li><li>Aging<\/li><li>Pressure\/tension<\/li><\/ul><\/li><li>Examples:<ul><li>Cerebral atrophy (due to aging or disease)<\/li><li>Muscle atrophy (due to prolonged bed rest)<\/li><\/ul><\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_2\">\n<h2 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Involution<\/h2>\n<\/span><span class=\"block-content\" id=\"contents_2\">\n\n\n<p class=\"wp-block-paragraph\">A general term for describing the shrinking of an organ.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>Characterized by both atrophy and programmed cell death (<strong>apoptosis<\/strong>)<\/li><li>Notable examples:<ul><li>Uterus after pregnancy<\/li><li>Thymus gland after puberty (replaced by adipose tissue &#8212; thymus adiposus)<\/li><li>Mammary glands after the end of breastfeeding<\/li><\/ul><\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_3\">\n<h2 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Apoptosis<\/h2>\n<\/span><span class=\"block-content\" id=\"contents_3\">\n\n\n<p class=\"wp-block-paragraph\">Defined as&nbsp;<strong>programmed cell death<\/strong>,&nbsp;in which the cells activate different enzymes in order to degrade its own nuclear DNA and its cytoplasmic proteins while keeping its membrane intact.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>The name apoptosis means \u201cfalling off\u201d, and is given due to the fragments that are formed during apoptosis<ul><li>Each of the cellular fragments is covered by the part of the cell&#8217;s membrane, meaning it remains intact<\/li><li>Because the membrane remains intact, apoptosis does not elicit inflammation<\/li><\/ul><\/li><li>Apoptosis is the main pathway of cell death during embryological development<\/li><li>Apoptosis serves two purposes, and plays a key factor in both physiological and pathological reactions:<ul><li>Elimination of <strong>potentially harmful<\/strong> cells (damaged, infected, or functionally impaired cells)<\/li><li>Elimination of <strong>exhausted<\/strong> cells that have \u201cserved their duties\u201d and are not able to perform efficiently enough<\/li><\/ul><\/li><li>Not-so-obvious examples include:<ul><li>Elimination of autoreactive immune cells (in the thymus)<\/li><li>Elimination of excessive leukocytes after inflammation<\/li><\/ul><\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_4\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Molecular pathway<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_4\">\n\n\n<p class=\"wp-block-paragraph\">The two molecular pathways of apoptosis activate cysteine protease&nbsp;enzymes (<strong>caspases<\/strong>) to perform their functions:<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li><strong>Mitochondrial pathway (intrinsic)<\/strong><ul><li>Predominant pathway<\/li><li>Increase in the permeability of the mitochondria leads to leakage of pro-apoptotic proteins<\/li><\/ul><\/li><li><strong>Death receptor pathway (extrinsic):<\/strong><ul><li>Takes place via <strong>death receptors<\/strong> belong to the tumor necrosis factor (TNF) receptor family<ul><li>These receptors consist of \u201cdeath domain\u201d which initiates the apoptotic signaling pathway<\/li><li>Type I TNF receptor and Fas receptor are the two main receptors belonging to this group<\/li><\/ul><\/li><\/ul><\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_5\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title3\">Mitochondrial pathway<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_5\">\n\n\n<p class=\"wp-block-paragraph\">As I mentioned before, the mitochondria are a key regulator of a cell&#8217;s survivability. When certain proteins leak out of it (namely <strong>cytochrome C<\/strong>),&nbsp; forming a complex (<strong>apoptosome<\/strong>) that triggers the <strong>caspase cascade&nbsp;<\/strong>via <strong>caspase-9<\/strong>, which together with other proteins and co-factors leads to apoptosis.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>Proteins that regulate mitochondrial membrane permeability are derived from <strong>Bcl-2<\/strong> protein<ul><li>This family of about 20 proteins has both anti-apoptotic members (<strong>Bcl-2<\/strong> itself) as well as pro-apoptotic members (<strong>Bax<\/strong> and <strong>Bak<\/strong>)<\/li><\/ul><\/li><li><strong>Bcl-2<\/strong> and <strong>Bcl-X<sub>L<\/sub><\/strong>&nbsp;(which related to Bcl-2) act to <strong>inhibit<\/strong>&nbsp;apoptosis<\/li><li><strong>Bak<\/strong> and <strong>Bax&nbsp;<\/strong>act to&nbsp;<strong>initiate<\/strong> it<\/li><li>The whole process begins with&nbsp;the activation of special sensors &#8212;&nbsp;<strong>BH3 proteins&nbsp;<\/strong>&#8212; who cause the dimerization of Bak and Bax which eventually lead to apoptosis (by the process described above)<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_6\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title3\">Death receptor pathway<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_6\">\n\n\n<p class=\"wp-block-paragraph\">The ligand of Fas receptor (FasL) is expressed mostly on the surface of activated T cells.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>The binding of FasL to FasR will activate adaptor proteins which will activate the caspase cascade via&nbsp;<strong>caspase-8<\/strong>, and as in the mitochondrial pathway, together with other proteins and co-factors leads to apoptosis.<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_7\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Clearance<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_7\">\n\n\n<p class=\"wp-block-paragraph\">Apoptotic cells produce &#8220;eat-me&#8221; signals, so nearby macrophages will know to clear them out and prevent inflammation. This is manifested in multiple ways, for example:<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>Secretion of certain cytokines<\/li><li>&#8220;Flipping over&#8221; of phosphatidylserine chains (which are normally presented towards the inner leaflet)<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_8\">\n<h2 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Other forms of cell death<\/h2>\n<\/span><span class=\"block-content\" id=\"contents_8\">\n\n\n<ul class=\"wp-block-list\"><li><strong>Necroptosis<\/strong><ul><li>TNF receptors (among others) activate kinases that result in death very similar to necrosis<\/li><li>Might be related to immune responses and ischemic injuries<\/li><\/ul><\/li><li><strong>Pyroptosis<\/strong><ul><li>Activates caspases via a complex called&nbsp;<strong>inflammasome<\/strong><\/li><li>Might be related to immune response.<\/li><\/ul><\/li><\/ul>\n<\/span><div id=\"the_titles\" style=\"display:none;\"><h2 class=\"wp-block-heading\" class=\"wp-block-heading\">Atrophy<\/h2><h2 class=\"wp-block-heading\" class=\"wp-block-heading\">Involution<\/h2><h2 class=\"wp-block-heading\" class=\"wp-block-heading\">Apoptosis<\/h2><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">Molecular pathway<\/h3><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Mitochondrial pathway<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Death receptor pathway<\/h4><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">Clearance<\/h3><h2 class=\"wp-block-heading\" class=\"wp-block-heading\">Other forms of cell death<\/h2><\/div>","protected":false},"excerpt":{"rendered":"<p>Atrophy An adaptive response characterized by decreased protein synthesis and increased protein degradation. Cells decrease in size Degradation of proteins using: Lysosomes Ubiquitin-proteasome pathway Autophagy &#8220;Self-eating&#8221; Natural, regulated mechanism of the cell that disassembles unnecessary or dysfunctional components Elimination of intracellular substances Membrane-bound vacuoles containing mitochondria, ER, complex protein fragments and undegradable substances Undegradable substances [&hellip;]<\/p>\n","protected":false},"author":275,"featured_media":0,"parent":7074,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":""},"class_list":["post-7076","page","type-page","status-publish","hentry"],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v28.0 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Atrophy, Involution and apoptosis &#8211; Meddists<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/meddists.com\/learn\/pre-clinical\/pathology\/cell-injury-cell-death-and-adaptation\/adaptation\/atrophy-involution-and-apoptosis\/\" \/>\n<meta name=\"twitter:label1\" content=\"Est. reading time\" \/>\n\t<meta name=\"twitter:data1\" content=\"3 minutes\" \/>\n<script type=\"application\/ld+json\" class=\"yoast-schema-graph\">{\"@context\":\"https:\\\/\\\/schema.org\",\"@graph\":[{\"@type\":\"WebPage\",\"@id\":\"https:\\\/\\\/meddists.com\\\/learn\\\/pre-clinical\\\/pathology\\\/cell-injury-cell-death-and-adaptation\\\/adaptation\\\/atrophy-involution-and-apoptosis\\\/\",\"url\":\"https:\\\/\\\/meddists.com\\\/learn\\\/pre-clinical\\\/pathology\\\/cell-injury-cell-death-and-adaptation\\\/adaptation\\\/atrophy-involution-and-apoptosis\\\/\",\"name\":\"Atrophy, Involution and apoptosis &#8211; 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