Atrophy is a natural process in which specific organs or cells shrink. In humans, atrophy occurs at specific ages and under specific conditions. For example, adrenal glands shrink after birth due to a decrease in the inner cortex. The lymphoid tissues also shrink after birth, and the pineal gland at puberty tends to atrophy. Atrophic tissues form calcium deposits and are influenced by nutritional and blood supply changes.
Disuse
Disuse atrophy affects muscles and is often a result of immobility. For instance, if you cannot walk for a long time, your muscles will atrophy. This happens because you stop using specific muscle groups or many muscles throughout your body. The lack of use of these muscles can cause further weakness, making your muscle atrophy worse.
In most cases, muscle atrophy is reversible with exercise and a proper diet. However, in some cases, the muscle loss can be irreversible, and the recovery time can take many months.
Denervation
The mechanism underlying denervation-induced atrophy may include an increased generation of ROS in mitochondria. While this is an ongoing debate, these results support the notion that denervation leads to atrophy. Furthermore, these findings are not limited to humans. They also apply to the mouse model.
The leading causes of denervation atrophy include motor neuron diseases and peripheral neuropathies. The most common disorders affecting motor neuron tissue include amyotrophic lateral sclerosis (ALS) and autosomal recessive spinal muscular atrophy (ASMA). However, some arthropod-borne viruses can also cause denervation atrophy in some patients.
Genetics
Multiple system atrophy (MSA) is a rare neurodegenerative disorder characterized by intracellular accumulation of a-synuclein and loss of nerve cells in the striatonigral and olivopontocerebellar structures. Epidemiological studies suggest the involvement of autoimmune mechanisms in MSA pathogenesis, although the genetic etiology is unclear. In addition, researchers have identified shared genetic loci that appear to be associated with the disease, but their exact mechanisms remain unknown.
Molecular mechanisms of skeletal muscle atrophy are still poorly understood. However, current research shows that skeletal muscle atrophy is caused by a mutation in the survival motor neuron gene (SMN1). The mutations in this gene are associated with a wide range of phenotypic symptoms, including muscle weakness and atrophy. In some cases, the phenotype is so severe that the patient may die prematurely.
Injury to a cell
Cell injury can take several forms, including oxidative modification, DNA lesions, or lipid peroxidation. It may also involve apoptosis or cell death. In some cases, the injuries are reversible, but in others, they are irreversible. In either case, a cell will atrophy due to the depletion of ATP. This, in turn, results in an impaired ability of the cell to perform its normal functions.
Generally, cells change their morphology or function to compensate for external stressors. This helps them survive and function better in the new environment. The good news is that these changes are reversible if the stressor is removed. However, the effects of persistent exposure to an insult can be permanent.
Persistent pressure
Persistent pressure can cause the atrophy of organs, tissues, and cells in the body. Whether it is a benign tumor that is growing and causing pressure on the surrounding areas or an artery that has been dilated locally and is causing pressure on adjacent structures, atrophy can result.
This condition occurs when oxygen, blood, and nutrients are lost in muscles. In addition, the muscles become inactive and limp. This process can last for several weeks or even months. Finally, muscle fibers disappear, and the muscles are replaced by fat cells and loose connective tissue. Atrophy can also lead to contractures.
