{"id":6267,"date":"2026-05-27T21:21:01","date_gmt":"2026-05-28T01:21:01","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&#038;p=6267"},"modified":"2026-05-27T22:35:59","modified_gmt":"2026-05-28T02:35:59","slug":"outcomes-of-cell-injury","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/outcomes-of-cell-injury\/","title":{"raw":"Section 8 Outcomes of Cell Injury","rendered":"Section 8 Outcomes of Cell Injury"},"content":{"raw":"<span class=\"transcription-time-part\" style=\"text-align: initial;font-size: 1em\" data-time-start=\"1537.339\" data-time-end=\"1539.71\">When a cell is injured three possible outcomes exist. <\/span>\r\n<ul>\r\n \t<li><strong>Recovery:<\/strong>\u00a0 The injury is reversible.\u00a0 The stressor is removed, the cell repairs itself, and normal function is restored.<\/li>\r\n \t<li><strong>Apoptosis:<\/strong>\u00a0 The cell's internal machinery determines that damage is too severe to repair, and the cell undergoes clean, programmed death.<\/li>\r\n \t<li><strong>Unplanned cell death:<\/strong>\u00a0 The cell is overwhelmed and ruptures, causing inflammation and potential collateral damage to surrounding tissue.\r\n<ul>\r\n \t<li><strong>Necrosis:<\/strong>\u00a0 The premature death of a group of neighbouring cells or entire sections of tissue is referred to as necrosis.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<div class=\"textbox textbox--key-takeaways\"><header class=\"textbox__header\">\r\n<p class=\"textbox__title\"><strong>Interesting Finding:\u00a0 Cell Death During Heart Attacks<\/strong><\/p>\r\n\r\n<\/header>\r\n<div class=\"textbox__content\">\r\n\r\nResearch into myocardial infarction (heart attack) has found that approximately <strong>80% of cell death<\/strong> is apoptotic, and only<strong> 20% is necrotic<\/strong>.\u00a0 This means that the majority of hear cells sense low oxygen levels and deliberately undergo programmed death rather than bursting.\u00a0 This is clinically significant:\u00a0 apoptosis attracts fewer white blood cells, produces less ROS-mediated collateral damage, and actually speeds up healing relative to necrosis.\r\n\r\n<\/div>\r\n<\/div>","rendered":"<p><span class=\"transcription-time-part\" style=\"text-align: initial;font-size: 1em\" data-time-start=\"1537.339\" data-time-end=\"1539.71\">When a cell is injured three possible outcomes exist. <\/span><\/p>\n<ul>\n<li><strong>Recovery:<\/strong>\u00a0 The injury is reversible.\u00a0 The stressor is removed, the cell repairs itself, and normal function is restored.<\/li>\n<li><strong>Apoptosis:<\/strong>\u00a0 The cell&#8217;s internal machinery determines that damage is too severe to repair, and the cell undergoes clean, programmed death.<\/li>\n<li><strong>Unplanned cell death:<\/strong>\u00a0 The cell is overwhelmed and ruptures, causing inflammation and potential collateral damage to surrounding tissue.\n<ul>\n<li><strong>Necrosis:<\/strong>\u00a0 The premature death of a group of neighbouring cells or entire sections of tissue is referred to as necrosis.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<div class=\"textbox textbox--key-takeaways\">\n<header class=\"textbox__header\">\n<p class=\"textbox__title\"><strong>Interesting Finding:\u00a0 Cell Death During Heart Attacks<\/strong><\/p>\n<\/header>\n<div class=\"textbox__content\">\n<p>Research into myocardial infarction (heart attack) has found that approximately <strong>80% of cell death<\/strong> is apoptotic, and only<strong> 20% is necrotic<\/strong>.\u00a0 This means that the majority of hear cells sense low oxygen levels and deliberately undergo programmed death rather than bursting.\u00a0 This is clinically significant:\u00a0 apoptosis attracts fewer white blood cells, produces less ROS-mediated collateral damage, and actually speeds up healing relative to necrosis.<\/p>\n<\/div>\n<\/div>\n","protected":false},"author":1370,"menu_order":10,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":["zoe-soon"],"pb_section_license":"cc-by-nc-sa"},"chapter-type":[],"contributor":[60],"license":[57],"class_list":["post-6267","chapter","type-chapter","status-web-only","hentry","contributor-zoe-soon","license-cc-by-nc-sa"],"part":3,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/6267","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/users\/1370"}],"version-history":[{"count":2,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/6267\/revisions"}],"predecessor-version":[{"id":6305,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/6267\/revisions\/6305"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/parts\/3"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/6267\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=6267"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=6267"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=6267"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=6267"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}