Cellular Adaptations
Cells can undergo reversible changes in size, number, phenotype, metabolic activity, or functional state in response to environmental changes. These adaptations commonly include:
- Hypertrophy
- Hyperplasia
- Atrophy
- Metaplasia
Hypertrophy
- Definition: Increase in cell size leading to an increase in organ size
- Characteristics:
- No new cells, just larger cells
- Caused by the synthesis of more structural components
- Occurs in cells with increased functional demands or hormone stimulation
- Types:
- Physiological (e.g., muscle growth in bodybuilders)
- Pathological (e.g., cardiac hypertrophy from hypertension or valve incompetence)
- Mechanisms:
- Mechanical sensors activated by workload
- Growth factors (e.g., TGF-beta, IGF-1)
- Vasoactive agents (e.g., endothelin-1, angiotensin II)
- Signal transduction pathways: PI3K/Akt (physiological) & GPCR (pathological)
- Switchover to fetal/neonatal proteins in some cases
Hyperplasia
- Definition: Increase in the number of cells, increasing organ or tissue size
- Characteristics:
- Occurs in dividing cells
- Frequently coexists with hypertrophy
- Types:
- Physiological: Hormonal (e.g., breast tissue in pregnancy), Compensatory (e.g., liver regeneration)
- Pathological: Often due to excess hormones/growth factors (e.g., endometrial hyperplasia, benign prostatic hyperplasia)
- Mechanism: Doesn't involve mutations in genes regulating cell division, distinct from cancer
Atrophy
- Definition: Decrease in cell size and/or number, reducing organ/tissue size
- Types:
- Physiological: Common in early development (e.g., ductus arteriosus), later life (e.g., thymus involution)
- Pathological: Can be generalized (e.g., starvation, senile atrophy) or localized (e.g., disuse, denervation, pressure atrophy)
- Mechanisms:
- Decreased protein synthesis & increased degradation (ubiquitin-proteasome pathway)
- Increased autophagy (cell self-digestion for survival)
Metaplasia
- Definition: Replacement of one differentiated cell type by another
- Types:
- Epithelial Metaplasia: Common is squamous metaplasia (e.g., respiratory tract from cigarette smoking)
- Detective Tissue Metaplasia: Formation of cartilage, bone in unusual locations (e.g., bone in muscle)
- Mechanism: Reprogramming of stem cells via cytokines, growth factors, and extracellular matrix components, not transdifferentiation
- Consequences: Loss of original cell function, potential for malignant transformation if stimulus persists