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Cellular adaptation

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Title: Cellular adaptation  
Author: World Heritage Encyclopedia
Language: English
Subject: Pathology, Necrosis, Clinical virology, Lipochrome, Glandular metaplasia
Collection: Cell Biology
Publisher: World Heritage Encyclopedia

Cellular adaptation

In cell biology and pathophysiology, cellular adaptation refers to changes made by a cell in response to adverse environmental changes.[1] The adaptation may be physiologic(al) (normal) or pathologic(al) (abnormal). Five major types of adaptation include atrophy, hypertrophy, hyperplasia, dysplasia, and metaplasia.


  • Atrophy 1
  • Hypertrophy 2
  • Hyperplasia 3
  • Metaplasia 4
  • Dysplasia 5
  • Notes and references 6


Atrophy is a decrease in cell size. If enough cells in an organ atrophy the entire organ will decrease in size. brain.


Hypertrophy is an increase in cell size. If enough cells of an organ hypertrophy so will the whole organ. The heart and kidneys have increased susceptibility to hypertrophy. Hypertrophy involves an increase in intracellular protein rather than cytosol (intracellular fluid). Hypertrophy may be caused by mechanical signals (e.g., stretch) or trophic signals (e.g., growth factors). An example of physiologic hypertrophy is in skeletal muscle with sustained weight bearing exercise. An example of pathologic hypertrophy is in cardiac muscle as a result of hypertension.


Hyperplasia is an increase in the number of cells. It is the result of increased cell estrogen. For example, the estrogen-dependent uterine cells undergo hyperplasia and hypertrophy following pregnancy. Pathologic hyperplasia is an abnormal increase in cell division. A common pathologic hyperplasia in women occurs in the endometrium and is called endometriosis.


Metaplasia occurs when a differentiated cell of a certain type is replaced by another cell type, which may be less differentiated. It is a reversible process thought to be caused by stem cell reprogramming. Stem cells are found in epithelia and embryonic mesenchyme of connective tissue. A prominent example of metaplasia involves the changes associated with the respiratory tract in response to inhalation of irritants, such as smog or smoke. The bronchial cells convert from mucus-secreting, ciliated, columnar epithelium to non-ciliated, squamous epithelium incapable of secreting mucus. These transformed cells may become dysplasic or cancerous if the stimulus (e.g., cigarette smoking) is not removed. The most common example of metaplasia is Barrett's esophagus, when the non-keratinizing squamous epithelium of the esophagus undergoes metaplasia to become mucinous columnar cells, ultimately protecting the esophagus from acid reflux originating in the stomach. If stress persists, metaplasia can progress to dysplasia and eventually carcinoma; Barrett's esophagus, for example, can eventually progress to adenocarcinoma of the esophagus if not treated.


Dysplasia refers generally to abnormal changes in cellular shape, size, and/or organization. Dysplasia is not considered a true adaptation; rather, it is thought to be related to hyperplasia and is sometimes called "atypical hyperplasia." Tissues prone to dysplasia include cervical and respiratory epithelicurs in the vicinity of cancerous cells, and it may be involved in the development of breast cancer. Although dysplasia is reversible, if stress persists, then dysplasia progresses to irreversible carcinoma.

Notes and references

  1. ^ Huether, S. E. & McCance, K. L. (2008). Understanding Pathophysiology, Ed 4, p. 62-65.
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