Page 14 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

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The GF receptors are activated (usually tyro- ers, nerve cells in adults. The capability of re-
sine kinase activity; → p. 7f., A10), which re- generation of an adult’s cardiac and skeletal
sults in phosphorylation of a number of pro- muscle cells is also very limited (→ e.g., myo-
teins. Lastly, the signaling cascade reaches the cardial infarction; p. 220).
nucleus, DNA synthesis is stimulated and the Adaptation to changed physiological or un-
cell divides (→ p.14). physiological demands can be achieved
In addition to tissue-specific growth factors through an increase or decrease in the number
(e.g., hepatic growth factor [HGF] in the liver), of cells (hyperplasia or aplasia; → D, E). This
there are those with a wider spectrum of ac- can be triggered by hormones (e.g., develop-
tion, namely epidermal growth factor (EGF), ment of secondary sex characteristics and
transforming growth factor (TGF-α), platelet- growth of mammary epithelium during preg-
derived growth factor (PDGF), fibroblast nancy) or can serve the process of compensa-
growth factor (FGF) as well as certain cyto- tion, as in wound healing or after reduction of
kines such as interleukin 1 and tumor necrosis liver parenchyma (→ B). Cell size may either
factor (TNF). Growth inhibition (→ p.14) oc- increase (hypertrophy), or decrease (atrophy)
curs, for example, in an epithelium in which a (→ E). This adaptation, too, can be triggered
gap has been closed by cell division, when
hormonally, or by an increase or decrease in
Fundamentals neighboring cells come into contact with one demand. While the uterus grows during preg-
nancy by both hyperplasia and hypertrophy,
another (contact inhibition). Even compensa-
skeletal and cardiac muscles can increase their
tory growth in the liver stops (→ B) when the
original organ mass has been regained. TGF-β
strength only by hypertrophy. Thus, skeletal
building) or atrophy from disuse (e.g., leg mus-
sponsible for this growth regulation.
1 and interferon-β are among the signals re- muscles hypertrophy through training (body-
The regeneration of labile and stable cells cle in a plaster cast after fracture or due to loss
does not necessarily mean that the original tis- of innervation). Cardiac hypertrophy develops
sue structure is reconstituted. For this to hap- normally in athletes requiring a high cardiac
pen the extracellular matrix must be intact, as output (cycling, cross-country skiing), or ab-
it serves as the guiding system for the shape, normally, for example, in hypertensives
growth, migration, and differentiation of the (→ p. 208ff.). Atrophied cells are not dead;
cell (→ C). The extracellular matrix consists of they can be reactivated—with the exception of
fibrous structural proteins (collagen I, II–V; permanent cells (brain atrophy). However,
elastin) and an intercellular matrix of glyco- similar signal pathways lead to atrophy and
proteins (e.g., fibronectin and laminin) that to “programmed cell death” or apoptosis
are embedded in a gel of proteoglycans and (→ p.12), so that an increased number of cells
glucosaminoglycans. The extracellular matrix may die in an atrophic tissue (→ D).
borders on epithelial, endothelial, and smooth Metaplasia is a reversible transformation of
muscle cells in the form of basal lamina (→ E). one mature cell type into another (→ E). This,
Integrins are proteins of the cell membrane too, is usually an adaptive course of events.
that connect the extracellular matrix with the The transitional epithelium of the urinary
intracellular cytoskeleton and transmit signals bladder, for example, undergoes metaplasia to
for the growth, migration, and differentiation squamous epithelium on being traumatized by
of the cell to the cell interior (→ C). If, as hap- kidney stones, and so does esophageal epi-
pens in severe tissue damage, the matrix is ex- thelium in reflux esophagitis (→ p.136ff.), or
tensively destroyed (e.g., in a deep gastric ul- ciliated epithelium of the respiratory tract in
cer [→ p.144ff.] or large skin wound), the orig- heavy smokers. The replacement epithelium
inal tissue is replaced by scar tissue. In this may better withstand unphysiological de-
case otherwise resting cells of the connective mands, but the stimuli that sustain lasting
tissue and mesenchyme also proliferate (see metaplasia can also promote the development
above). of tumor cells (→ p.14).
When so-called permanent cells have died
4 they cannot be replaced, because they are un-
able to divide. Such cells include, among oth-
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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