Victor Forge
Chemotherapy is a widely used treatment for cancer, but it can also cause several side effects, including muscle weakness. This is a well-known clinical problem that can drastically impair a patient's quality of life and worsen survival outcomes. The molecular mechanisms behind chemotherapy-induced muscle weakness are complex and not yet fully understood, but researchers are working to unravel them and develop more effective treatments. This paragraph will explore the available scientific evidence on the link between chemotherapy and muscle weakness, the underlying causes, and potential interventions.
| Characteristics | Values |
|---|---|
| Does chemo weaken muscles? | Yes |
| Drugs that cause muscle weakness | Doxorubicin, Folfiri, Cisplatin |
| Effects | Fatigue, Falls, Fractures, Increased Mortality |
| Mechanism | Oxidative Stress, Calcium Cycle Disruption, Loss of Motor Unit Connectivity |
| Treatments | None Currently Approved, Research Ongoing |
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What You'll Learn
Chemotherapy-induced peripheral neuropathy (CIPN)
The risk of developing CIPN depends on the type of chemotherapy and the dose given, with certain classes of chemotherapy drugs being more likely to cause nerve damage than others. The drugs most commonly associated with CIPN are used to treat prevalent cancer types, including breast cancer, colon cancer, lung cancer, and prostate cancer. Platinum drugs, such as cisplatin, carboplatin, and oxaliplatin, are among the more common chemotherapy medications that can induce CIPN.
Currently, there is no known method to completely prevent CIPN. However, early treatment can help reduce its severity and impact. If CIPN becomes severe, doctors may need to adjust the chemotherapy regimen. Some studies suggest that cryotherapy, which involves cooling the hands and feet during chemotherapy infusions, may reduce the occurrence of CIPN, particularly in patients receiving taxane-based chemotherapy. Acupuncture has also been proposed as a potential therapy to alleviate CIPN symptoms.
The underlying mechanisms of CIPN are complex, involving peripheral, spinal, and supraspinal changes. These changes include alterations in sodium and potassium channel expression and activity, mitochondrial dysfunction, and immune cell interactions. A better understanding of these mechanisms is crucial for developing more effective management strategies and targeted treatments for CIPN.
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Doxorubicin's effect on calcium availability
Chemotherapy drugs can damage the nerves that send signals between the central nervous system and the limbs, causing muscle weakness in the legs. This is known as chemotherapy-induced peripheral neuropathy (CIPN).
Doxorubicin is a widely used chemotherapy medication for treating cancer. It is one of the most effective anti-neoplastic drugs. However, its clinical utility is limited by its associated cardiotoxicity, specifically cardiac contractile dysfunction.
Doxorubicin-induced tension development is blunted by ruthenium red, an inhibitor of the ryanodine receptor, suggesting that doxorubicin alters calcium availability. Studies have shown that isolated skeletal muscle sarcoplasmic reticulums exposed to doxorubicin exhibit increased calcium release. This is in line with another study that found increased calcium influx in C2C12 myotubes exposed to doxorubicin. The data suggests that doxorubicin acts similarly to caffeine, sensitising the ryanodine receptor to activation calcium and stimulating calcium release.
Furthermore, studies on the effects of doxorubicin on vascular smooth muscle have observed apoptotic changes and confirmed apoptotic phenomena through DNA fragmentation in isolated bovine aortic endothelial cells (BAECs) and A7r5 vascular smooth muscle cells. These findings suggest that doxorubicin may be a general depressant of muscle function.
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Loss of motor unit connectivity
Skeletal muscle wasting and weakness caused by cancer and its treatments, known as "cachexia", drastically impair quality of life and worsen survival outcomes in cancer patients. There are currently no approved treatments for cachexia. Hence, further investigation into the causes of cachexia induced by cancer and chemotherapy is necessary.
Motor units are functional units made up of a motor neuron and all the myofibers it innervates. Loss of motor unit number, as suggested by motor unit number estimation (MUNE), has been shown to precede loss of muscle strength and is correlated with muscle weakness and atrophy in aging rodents. Investigations into changes in motor unit number in cachexia have not occurred, leaving a gap in understanding the mechanisms that contribute to muscle weakness caused by cancer and chemotherapy.
To address this, an established MUNE technique was used to gain insight into the number of motor neurons functionally connected to the triceps surae muscles of the mouse hindlimb. Taking advantage of three colorectal cancer (CRC) cell lines (C26, MC38, and HCT116) and two chemotherapeutic regimens (folfiri and cisplatin) known to induce cachexia, alterations of MUNE were assessed to investigate whether muscle wasting and weakness were associated with a loss of motor unit number.
The findings indicate that loss of motor unit number is associated with muscle wasting and muscle weakness caused by cancer and chemotherapy. Cachexia induced by cancer and its treatments is accompanied by a loss of NMJ-associated proteins and abnormal presynaptic morphology, further suggestive of altered innervation.
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Oxidative stress
Chemotherapy can cause muscle weakness and fatigue, which can persist for months or years after treatment. This can lead to problems such as falls, which can result in fractures and even increased mortality.
One of the underlying mechanisms of muscle weakness in chemotherapy-treated patients is a developed state of oxidative stress. This is defined as a disruption of redox signalling and control. Chemotherapeutic agents can directly or indirectly produce a state of oxidative stress. Drugs that include a quinone moiety in their chemical structure can directly produce a state of oxidative stress by interacting with molecular oxygen and undergoing redox cycling, leading to the generation of reactive oxygen species (ROS).
Other chemotherapeutic agents can indirectly produce a state of oxidative stress by decreasing antioxidant levels, crippling the cell's defences against elevated oxidants. Circulating biomarkers are a nonspecific systemic index of oxidative stress in the body. In cancer patients undergoing treatment, circulating markers of oxidative stress, in the form of lipid peroxidation and protein carbonyl content, are elevated.
Doxorubicin, for example, can directly stimulate an increase in oxidants by undergoing redox cycling. However, a secondary, indirect method for doxorubicin to stimulate oxidants is via an inflammatory response. Doxorubicin-treated animals and patients exhibit a stress response, characterised by an increase in serum levels of inflammatory cytokines, especially TNF (a pro-inflammatory cytokine produced by many cell types, including cardiac and skeletal myocytes).
In skeletal muscle, exposure to elevated oxidants is known to cause muscle weakness and accelerate the rate of fatigue. Antioxidant exposure delays the rate of fatigue, supporting this connection. Chemotherapy-induced oxidative stress in cancer patients could be a reflection of elevated muscle-derived oxidants, an underlying mechanism for the muscle weakness experienced by patients.
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Cancer-induced bone resorption
Cancer treatments, including chemotherapy and radiation, have been linked to bone loss and an increased risk of osteoporosis and fractures. This bone loss is attributed to cellular senescence, a process where cells permanently stop dividing but remain active, releasing substances that affect neighbouring cells. In the case of bones, senescent cells disrupt the normal process of bone remodelling, which involves osteoclasts breaking down old bone and osteoblasts building new bone. When this balance is disrupted, bones can become thinner and weaker, leading to osteoporosis and an increased risk of fractures.
One specific chemotherapy drug, doxorubicin, has been associated with bone loss in breast cancer bone metastases. The mechanism involves the interplay between oxidative stress and the induction of TGFβ. Additionally, breast cancer cells can undergo an epithelial-mesenchymal transition, stimulated by cancer-associated fibroblasts, and subsequently express osteoblast cadherin CDH11, RUNX2, osteonectin (SPARC), and the bone matrix-remodelling protein periostin, further contributing to bone degradation.
Understanding the mechanisms of cancer-induced bone resorption is crucial for developing effective treatments. For example, the tyrosine kinase inhibitor cabozantinib has shown promising results in targeting bone osteoblasts and reducing prostate cancer cell proliferation in bones. Additionally, investigational drugs have been found to block molecular signals from senescent cells that disrupt bone remodelling, which could potentially prevent chemotherapy-induced bone loss.
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Frequently asked questions
Yes, chemotherapy can cause muscle weakness, which can persist for months or years after treatment. This can be caused by a state of oxidative stress, which affects nontargeted tissues such as striated muscle.
The exact mechanisms are still being studied, but it is thought that the release of too much TGFβ from bone disrupts the normal calcium cycle needed for muscle contraction. This can be caused by certain chemotherapy drugs, such as doxorubicin, which alter calcium availability.
Muscle weakness can cause several issues, including fatigue and falls, which can lead to fractures and increased mortality. It can also be associated with cachexia, a condition characterized by weight loss, depletion of fat and muscle, and reduced quality of life.
