scholarly journals Toll-Like Receptors in Ischaemia and Its Potential Role in the Pathophysiology of Muscle Damage in Critical Limb Ischaemia

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Hemanshu Patel ◽  
Sidney G. Shaw ◽  
Xu Shi-Wen ◽  
David Abraham ◽  
Daryll M. Baker ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Potential Role ◽  
Arterial Disease ◽  
Severe Form ◽  
Tissue Loss ◽  
Critical Limb Ischaemia ◽  
Limb Ischaemia ◽  
Toll Like Receptors ◽  
Skeletal Muscle Damage

Toll-like receptors (TLRs) are key receptors of the innate immune system which are expressed on immune and nonimmune cells. They are activated by both pathogen-associated molecular patterns and endogenous ligands. Activation of TLRs culminates in the release of proinflammatory cytokines, chemokines, and apoptosis. Ischaemia and ischaemia/reperfusion (I/R) injury are associated with significant inflammation and tissue damage. There is emerging evidence to suggest that TLRs are involved in mediating ischaemia-induced damage in several organs. Critical limb ischaemia (CLI) is the most severe form of peripheral arterial disease (PAD) and is associated with skeletal muscle damage and tissue loss; however its pathophysiology is poorly understood. This paper will underline the evidence implicating TLRs in the pathophysiology of cerebral, renal, hepatic, myocardial, and skeletal muscle ischaemia and I/R injury and discuss preliminary data that alludes to the potential role of TLRs in the pathophysiology of skeletal muscle damage in CLI.

scholarly journals Toll-like receptors 2 and 6 mediate apoptosis and inflammation in ischemic skeletal myotubes

2019 ◽  
Vol 24 (4) ◽  
pp. 295-305 ◽  
Author(s):  
Hemanshu Patel ◽  
Cissy Yong ◽  
Ali Navi ◽  
Sidney G Shaw ◽  
Xu Shiwen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Signaling Pathway ◽  
Muscle Damage ◽  
Limb Ischemia ◽  
Therapeutic Benefit ◽  
Toll Like Receptors ◽  
Tlr Signaling ◽  
Skeletal Muscle Damage ◽  
Tlr Signaling Pathway

Critical limb ischemia (CLI) is associated with skeletal muscle damage. However, the pathophysiology of the muscle damage is poorly understood. Toll-like receptors (TLR) have been attributed to play a role in ischemia-induced tissue damage but their role in skeletal muscle damage in CLI is unknown. TLR2 and TLR6 expression was found to be upregulated in skeletal muscle of patients with CLI. In vitro, ischemia led to upregulation of TLR2 and TLR6 by myotubes, and activation of the downstream TLR signaling pathway. Ischemia-induced activation of the TLR signaling pathway led to secretion of the pro-inflammatory cytokine interleukin-6 and muscle apoptosis, which were abrogated by neutralising TLR2 and TLR6 antibodies. Our study demonstrates that TLR2 and TLR6 are upregulated in ischemic muscle and play a role in ischemia-induced muscle damage. Thus, manipulating the TLR pathway locally may be of potential therapeutic benefit.

scholarly journals Endovascular management of Critical Limb Ischaemia: Study of 100 Cases

2019 ◽  
Vol 12 (1) ◽  
pp. 40-44
Author(s):  
Md Humayun Kabir ◽  
Munshi Md Mojibur Rahman ◽  
AKM Musa Khan ◽  
Rumman Idris
Keyword(s):  
Limb Ischemia ◽  
Major Amputation ◽  
Severe Form ◽  
Tissue Loss ◽  
Critical Limb Ischaemia ◽  
Military Hospital ◽  
Limb Ischaemia ◽  
Rest Pain ◽  
Excellent Outcome ◽  
Number Of Patients

Background: Critical limb ischemia (CLI) is the most severe form of Peripheral Artery Disease (PAD) and represents approximately 1% of the total number of patients with PAD. CLI is associated with a higher risk of limb loss in the absence of revascularization. Objectives of the study are to find out the modality of treatment in CLI, different types of endovascular therapy in CLI and their outcome. Methods: A retrospective study evaluated 100 patients with CLI reported to cardiovascular surgery department in Combined Military Hospital (CMH), Dhaka between July 2016 to June 2018. Patients with disabling claudication or rest pain and tissue loss are included in the study. All patients were evaluated by peripheral angiogram and revascularisation of limbs was done by endovascular procedure in 79 patients, by surgical intervention in 12 patients. Results: Forty-four patients (44%) presented with rest pain and disabling claudication, 56 patients (56%) presented with tissue loss. Revascularization of limbs was done in 91 patients (93%). No intervention could be done in 9 patients (9%). Endovascular interventions were done in 79 patients (87%). Twelve patients (13%) underwent surgical bypass. All patients with rest pain remains asymptomatic in 6 months follow up; 2 patients developed reocclusion within 1 year. No major amputation in patients with only rest pain. Conclusion: Revascularization is the main modality of treatment in CLI. Most of the patient can be treated by endovascular percuteneous procedure. Early intervention in CLI patient without tissue loss carries excellent outcome. Cardiovasc. j. 2019; 12(1): 40-44

Cardiorespiratory and skeletal muscle damage due to COVID-19: making the urgent case for rehabilitation

2021 ◽  
pp. 1-14
Author(s):  
Rebeca Nunes Silva ◽  
Cássia Da Luz Goulart ◽  
Murilo Rezende Oliveira ◽  
Guilherme Yassuyuki Tacao ◽  
Guilherme Dionir Back ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Skeletal Muscle Damage ◽  
Urgent Case

Modifications in the Concentrations of Circulating Myoglobin after Treatment with Low Doses of Adriamycin

1985 ◽  
Vol 71 (5) ◽  
pp. 463-468 ◽  
Author(s):  
Giovanni Carulli ◽  
Aldo Clerico ◽  
Alessandra Marini ◽  
Maria Grazia Del Chicca ◽  
Renato Vanacore ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Cancer Patients ◽  
Muscle Damage ◽  
Low Doses ◽  
Skeletal Muscle Damage ◽  
Creatine Kinase Mb

The modifications in the concentration of circulating myoglobin have been studied by means of a radioimmunoassay in 15 cancer patients undergoing polychemotherapy including adriamycin. In 8 patients significant increases in myoglobin levels were found after injection of low doses of the drug (25-50 mg/m2). Moreover, a disturbance of the normal biorhythm of the protein was evident in 12 patients. Creatine kinase-MB was evaluated by means of a radioimmunoassay, but there was no relation between an increase in the isoenzyme and an increase in myoglobin. No ECG modifications were detected. These data indicate that the measurement of myoglobin may offer an indication of myocardial or skeletal muscle damage caused by adriamycin.

Isoform specific ALT measurement during liver and skeletal muscle damage

2012 ◽  
Vol 211 ◽  
pp. S48
Author(s):  
Björn Glinghammar ◽  
Ingalill Rafter ◽  
Ina Schuppe-Koistinen ◽  
Ian Cotgreave
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Skeletal Muscle Damage

scholarly journals Hormone therapy attenuates exercise-induced skeletal muscle damage in postmenopausal women

2009 ◽  
Vol 107 (3) ◽  
pp. 853-858 ◽  
Author(s):  
Christina M. Dieli-Conwright ◽  
Tanya M. Spektor ◽  
Judd C. Rice ◽  
E. Todd Schroeder
Keyword(s):  
Skeletal Muscle ◽  
Hormone Therapy ◽  
Mrna Expression ◽  
Postmenopausal Women ◽  
Muscle Damage ◽  
Exercise Bout ◽  
Control Group ◽  
Skeletal Muscle Damage ◽  
Tnf Α ◽  
Exercise Induced

Hormone therapy (HT) is a potential treatment to relieve symptoms of menopause and prevent the onset of disease such as osteoporosis in postmenopausal women. We evaluated changes in markers of exercise-induced skeletal muscle damage and inflammation [serum creatine kinase (CK), serum lactate dehydrogenase (LDH), and skeletal muscle mRNA expression of IL-6, IL-8, IL-15, and TNF-α] in postmenopausal women after a high-intensity resistance exercise bout. Fourteen postmenopausal women were divided into two groups: women not using HT (control; n = 6, 59 ± 4 yr, 63 ± 17 kg) and women using traditional HT (HT; n = 8, 59 ± 4 yr, 89 ± 24 kg). Both groups performed 10 sets of 10 maximal eccentric repetitions of single-leg extension on the Cybex dynamometer at 60°/s with 20-s rest periods between sets. Muscle biopsies of the vastus lateralis were obtained from the exercised leg at baseline and 4 h after the exercise bout. Gene expression was determined by RT-PCR for IL-6, IL-8, IL-15, and TNF-α. Blood draws were performed at baseline and 3 days after exercise to measure CK and LDH. Independent t-tests were performed to test group differences (control vs. HT). A probability level of P ≤ 0.05 was used to determine statistical significance. We observed significantly greater changes in mRNA expression of IL-6, IL-8, IL-15, and TNF-α ( P ≤ 0.01) in the control group compared with the HT group after the exercise bout. CK and LDH levels were significantly greater after exercise ( P ≤ 0.01) in the control group. Postmenopausal women not using HT experienced greater muscle damage after maximal eccentric exercise, indicating a possible protective effect of HT against exercise-induced skeletal muscle damage.

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