A 9-wk docosahexaenoic acid-enriched supplementation improves endurance exercise capacity and skeletal muscle mitochondrial function in adult rats

2016 ◽  
Vol 310 (3) ◽  
pp. E213-E224 ◽  
Author(s):  
Marie Le Guen ◽  
Valérie Chaté ◽  
Isabelle Hininger-Favier ◽  
Brigitte Laillet ◽  
Béatrice Morio ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Docosahexaenoic Acid ◽  
Mitochondrial Function ◽  
Control Group ◽  
Placebo Control ◽  
Endurance Capacity ◽  
Adult Rats ◽  
Retention Capacity ◽  
Male Wistar Rats ◽  
And Function

Decline in skeletal muscle mass and function starts during adulthood. Among the causes, modifications of the mitochondrial function could be of major importance. Polyunsaturated fatty (ω-3) acids have been shown to play a role in intracellular functions. We hypothesize that docosahexaenoic acid (DHA) supplementation could improve muscle mitochondrial function that could contribute to limit the early consequences of aging on adult muscle. Twelve-month-old male Wistar rats were fed a low-polyunsaturated fat diet and were given DHA (DHA group) or placebo (control group) for 9 wk. Rats from the DHA group showed a higher endurance capacity (+56%, P < 0.05) compared with control animals. Permeabilized myofibers from soleus muscle showed higher O2 consumptions ( P < 0.05) in the DHA group compared with the control group, with glutamate-malate as substrates, both in basal conditions (i.e., state 2) and under maximal conditions (i.e., state 3, using ADP), along with a higher apparent Km for ADP ( P < 0.05). Calcium retention capacity of isolated mitochondria was lower in DHA group compared with the control group ( P < 0.05). Phospho-AMPK/AMPK ratio and PPARδ mRNA content were higher in the DHA group compared with the control group ( P < 0.05). Results showed that DHA enhanced endurance capacity in adult animals, a beneficial effect potentially resulting from improvement in mitochondrial function, as suggested by our results on permeabilized fibers. DHA supplementation could be of potential interest for the muscle function in adults and for fighting the decline in exercise tolerance with age that could imply energy-sensing pathway, as suggested by changes in phospho-AMPK/AMPK ratio.

scholarly journals Increase in the constrictor effects of Rho-kinase in skeletal muscle and coronary arteries of rats with chronic hypothyroidism

2018 ◽  
Vol 17 (4) ◽  
pp. 23-32
Author(s):  
D. K. Gaynullina ◽  
E. K. Selivanova ◽  
A. P. Sharova ◽  
O. S. Tarasova
Keyword(s):  
Skeletal Muscle ◽  
Gastrocnemius Muscle ◽  
Rho Kinase ◽  
Antithyroid Drug ◽  
Free Water ◽  
Control Group ◽  
Resistance Arteries ◽  
Adult Rats ◽  
Contractile Responses ◽  
Male Wistar Rats

Aim. The deficit of thyroid function is known to be accompanied by an increase in the overall peripheral vascular resistance. This work tested the hypothesis that long-term hypothyroidism leads to an increase in the vasoconstrictor effect of Rho-kinase in skeletal muscle and heart resistance arteries of adult rats.Materials and methods.Male Wistar rats consumed the antithyroid drug propylthiouracil (PTU) in drinking water (0.025%), starting at 10 weeks of age. The rats of the control group received PTU-free water. After 14 weeks, the contractile responses of the gastrocnemius muscle arteries (to the α1-adrenoceptor agonist methoxamine) and the septal coronary artery (to the thromboxane A2 receptor agonist U46619) were isometrically recorded. The contribution of the Rho-kinase to the arterial contractile responses was assessed using inhibitor Y27632 (3 μM).Results.The consumption of propylthiouracil was accompanied by a marked decrease of thyroid hormone concentrations and an increase in total cholesterol serum level as well as a decrease in body weight. Maximal contractile responses of studied arteries were also reduced in hypothyroid rats. However, basal tone and reactivity to the moderate concentrations of agonists in arteries of hypothyroid rats were increased compared to control animals. Y27632 significantly weakened the contractile responses of the arteries and negated the differences between the two groups of rats.Conclusion.Chronic hypothyroidism leads to an increase in the activity of the Rho-kinase signaling pathway in the arteries of the gastrocnemius muscle and heart, which results in the increase of the spontaneous tone of the arteries and their reactivity to agonists.

scholarly journals Atorvastatin impairs liver mitochondrial function in obese Göttingen Minipigs but heart and skeletal muscle are not affected

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Liselotte Bruun Christiansen ◽  
Tine Lovsø Dohlmann ◽  
Trine Pagh Ludvigsen ◽  
Ewa Parfieniuk ◽  
Michal Ciborowski ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Function ◽  
Citrate Synthase ◽  
Obese Group ◽  
Control Group ◽  
Dependent Manner ◽  
Respiratory Capacity ◽  
Protein Carbonyl Content ◽  
Functional Changes ◽  
Mitochondrial Respiratory

AbstractStatins lower the risk of cardiovascular events but have been associated with mitochondrial functional changes in a tissue-dependent manner. We investigated tissue-specific modifications of mitochondrial function in liver, heart and skeletal muscle mediated by chronic statin therapy in a Göttingen Minipig model. We hypothesized that statins enhance the mitochondrial function in heart but impair skeletal muscle and liver mitochondria. Mitochondrial respiratory capacities, citrate synthase activity, coenzyme Q10 concentrations and protein carbonyl content (PCC) were analyzed in samples of liver, heart and skeletal muscle from three groups of Göttingen Minipigs: a lean control group (CON, n = 6), an obese group (HFD, n = 7) and an obese group treated with atorvastatin for 28 weeks (HFD + ATO, n = 7). Atorvastatin concentrations were analyzed in each of the three tissues and in plasma from the Göttingen Minipigs. In treated minipigs, atorvastatin was detected in the liver and in plasma. A significant reduction in complex I + II-supported mitochondrial respiratory capacity was seen in liver of HFD + ATO compared to HFD (P = 0.022). Opposite directed but insignificant modifications of mitochondrial respiratory capacity were seen in heart versus skeletal muscle in HFD + ATO compared to the HFD group. In heart muscle, the HFD + ATO had significantly higher PCC compared to the HFD group (P = 0.0323). In the HFD group relative to CON, liver mitochondrial respiration decreased whereas in skeletal muscle, respiration increased but these changes were insignificant when normalizing for mitochondrial content. Oral atorvastatin treatment in Göttingen Minipigs is associated with a reduced mitochondrial respiratory capacity in the liver that may be linked to increased content of atorvastatin in this organ.

scholarly journals Diazepam attenuates the effects of cocaine on locomotion, 50-kHz ultrasonic vocalizations and phasic dopamine release in the nucleus accumbens of rats

2020 ◽  
Author(s):  
William N. Sanchez ◽  
Jose A. Pochapski ◽  
Leticia F. Jessen ◽  
Marek Ellenberger ◽  
Rainer K. Schwarting ◽  
...  
Keyword(s):  
Locomotor Activity ◽  
Nucleus Accumbens ◽  
Dopamine Release ◽  
Ultrasonic Vocalizations ◽  
Control Group ◽  
List Type ◽  
Adult Rats ◽  
Fast Scan Cyclic Voltammetry ◽  
Entire Duration ◽  
Male Wistar Rats

AbstractBackground and PurposeCurrently, no effective drug exists to treat cocaine use disorders, which affect millions of people worldwide. Benzodiazepines are potential therapeutic candidates, as microdialysis and voltammetry studies have shown that they can decrease dopamine release in the nucleus accumbens of rodents. In addition, we have recently shown that diazepam blocks the increase in dopamine release and the affective marker 50-kHz ultrasonic vocalizations (USV) induced by DL-amphetamine in rats.Experimental ApproachHere we tested whether administration of 2.5 mg·kg−1 diazepam (i.p.) in adult male Wistar rats could block the effects of 20 mg·kg−1 cocaine (i.p.) on electrically evoked phasic dopamine release in the nucleus accumbens measured by fast-scan cyclic voltammetry, as well as 50-kHz USV and locomotor activity.Key ResultsCocaine injection increased evoked dopamine release up to 3-fold within 5 min and the increase was significantly higher than baseline for at least 90 min. The injection of diazepam 15 min later attenuated the cocaine effect by nearly 50% and this attenuation was maintained for at least 30 min. Stimulant drugs, natural rewards and reward predictive cues are known to evoke 50-kHz USV in adult rats. In the present study, cocaine increased the number of 50-kHz USV of the flat, step, trill, and mixed kinds by 12-fold. This effect was at maximum 5 min after cocaine injection, decreased with time and lasted at least 40 min. Diazepam significantly blocked this effect for the entire duration of the session. The distance travelled by control rats during a 40-min session of exploration in an open field was at maximum in the first 5 min and decayed progressively until the end of the session. Cocaine-treated rats travelled significantly longer distances when compared to the control group, while diazepam significantly attenuated cocaine-induced locomotion by up to 50%.Conclusions and implicationThese results suggest that the neurochemical, affective, and stimulant effects of cocaine can be mitigated by diazepam.What is already knownDiazepam decreases dopamine release in the rodent nucleus accumbens (NAc) and reduces some effects produced by DL-amphetamine.What this study addsDiazepam attenuated the increase in phasic dopamine release caused by cocaine.Diazepam blocked the effect of cocaine on 50-kHz USV and locomotor activity.Clinical significanceThis study demonstrates that diazepam can block specific effects of cocaine that likely contribute to addiction.

Western diet in the perinatal period promotes dysautonomia in the offspring of adult rats

2016 ◽  
Vol 8 (2) ◽  
pp. 216-225 ◽  
Author(s):  
R. Vidal-Santos ◽  
F. N. Macedo ◽  
M. N. S. Santana ◽  
V. U. De Melo ◽  
J. L. de Brito Alves ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Systolic Arterial Pressure ◽  
Perinatal Period ◽  
Western Diet ◽  
Control Group ◽  
Standard Diet ◽  
Adult Rats ◽  
Male Wistar Rats ◽  
The Impact

The present study investigated the impact of a western diet during gestation and lactation on the anthropometry, serum biochemical, blood pressure and cardiovascular autonomic control on the offspring. Male Wistar rats were divided into two groups according to their mother’s diet received: control group (C: 18% calories of lipids) and westernized group (W: 32% calories of lipids). After weaning both groups received standard diet. On the 60th day of life, blood samples were collected for the analysis of fasting glucose and lipidogram. Cardiovascular parameters were measured on the same period. Autonomic nervous system modulation was evaluated by spectrum analysis of heart rate (HR) and systolic arterial pressure (SAP). The W increased glycemia (123±2v. 155±2 mg/dl), low-density lipoprotein (15±1v. 31±2 mg/dl), triglycerides (49±1v. 85±2 mg/dl), total cholesterol (75±2v. 86±2 mg/dl), and decreased high-density lipoprotein (50±4v. 38±3 mg/dl), as well as increased body mass (209±4v. 229±6 g) than C. Furthermore, the W showed higher SAP (130±4v. 157±2 mmHg), HR (357±10v. 428±14 bpm), sympathetic modulation to vessels (2.3±0.56v. 6±0.84 mmHg2) and LF/HF ratio (0.15±0.01v. 0.7±0.2) than C. These findings suggest that a western diet during pregnancy and lactation leads to overweight associated with autonomic misbalance and hypertension in adulthood.

scholarly journals Exercise-Induced Changes in Caveolin-1, Depletion of Mitochondrial Cholesterol, and the Inhibition of Mitochondrial Swelling in Rat Skeletal Muscle but Not in the Liver

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Damian Jozef Flis ◽  
Robert Antoni Olek ◽  
Jan Jacek Kaczor ◽  
Ewa Rodziewicz ◽  
Malgorzata Halon ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cholesterol Metabolism ◽  
Exercise Group ◽  
Mitochondrial Swelling ◽  
Control Group ◽  
Rat Skeletal Muscle ◽  
Muscle Mitochondria ◽  
Caveolin 1 ◽  
Male Wistar Rats ◽  
Exercise Induced

The reduction in cholesterol in mitochondria, observed after exercise, is related to the inhibition of mitochondrial swelling. Caveolin-1 (Cav-1) plays an essential role in the regulation of cellular cholesterol metabolism and is required by various signalling pathways. Therefore, the aim of this study was to investigate the effect of prolonged swimming on the mitochondrial Cav-1 concentration; additionally, we identified the results of these changes as they relate to the induction of changes in the mitochondrial swelling and cholesterol in rat skeletal muscle and liver. Male Wistar rats were divided into a sedentary control group and an exercise group. The exercised rats swam for 3 hours and were burdened with an additional 3% of their body weight. After the cessation of exercise, their quadriceps femoris muscles and livers were immediately removed for experimentation. The exercise protocol caused an increase in the Cav-1 concentration in crude muscle mitochondria; this was related to a reduction in the cholesterol level and an inhibition of mitochondrial swelling. There were no changes in rat livers, with the exception of increased markers of oxidative stress in mitochondria. These data indicate the possible role of Cav-1 in the adaptive change in the rat muscle mitochondria following exercise.

scholarly journals Forced internal desynchrony induces cardiometabolic alterations in adult rats

2019 ◽  
Vol 242 (2) ◽  
pp. 25-36
Author(s):  
Isis Gabrielli Barbieri de Oliveira ◽  
Marcos Divino Ferreira Junior ◽  
Paulo Ricardo Lopes ◽  
Dhiogenes Balsanufo Taveira Campos ◽  
Marcos Luiz Ferreira-Neto ◽  
...  
Keyword(s):  
Locomotor Activity ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Metabolic Response ◽  
Hepatic Metabolism ◽  
Control Group ◽  
Dark Cycle ◽  
Adult Rats ◽  
Internal Desynchronization ◽  
Male Wistar Rats ◽  
Experimental Group

Disruptions in circadian rhythms have been associated with several diseases, including cardiovascular and metabolic disorders. Forced internal desynchronization induced by a period of T-cycles of 22 h (T22 protocol) reaches the lower limit of entrainment and dissociates the circadian rhythmicity of the locomotor activity into two components, driven by different outputs from the suprachiasmatic nucleus (SCN). The main goal of this study was to evaluate the cardiovascular and metabolic response in rats submitted to internal desynchronization by T22 protocol. Male Wistar rats were assigned to either a control group subjected to a usual T-cycles of 24 h (12 h–12 h) or an experimental group subjected to the T22 protocol involving a 22-h symmetric light–dark cycle (11 h–11 h). After 8 weeks, rats subjected to the T22 exhibited desynchrony in their locomotor activity. Although plasma glucose and insulin levels were similar in both groups, desynchronized rats demonstrated dyslipidemia, significant hypertrophy of the fasciculate zone of the adrenal gland, low IRB, IRS2, PI3K, AKT, SOD and CAT protein expression and an increased expression of phosphoenolpyruvate carboxykinase in the liver. Furthermore, though they maintained normal baseline heart rates and mean arterial pressure levels, they also presented reduced baroreflex sensitivity. The findings indicate that circadian timing desynchrony following the T22 protocol can induce cardiometabolic disruptions. Early hepatic metabolism dysfunction can trigger other disorders, though additional studies are needed to clarify the causes.

scholarly journals PGC-1β prevents statin-associated myotoxicity in oxidative skeletal muscle

2017 ◽  
Author(s):  
François Singh ◽  
Joffrey Zoll ◽  
Urs Duthaler ◽  
Anne-Laure Charles ◽  
Gilles Laverny ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Rat Skeletal Muscle ◽  
Oxidative Defense ◽  
Muscle Types ◽  
And Function

AbstractStatins are generally well-tolerated, but can induce myopathy. Statins are associated with impaired expression of PGC-1β in human and rat skeletal muscle. The current study was performed to investigate the relation between PGC-1β expression and function and statin-associated myopathy. In WT mice, atorvastatin impaired mitochondrial function in glycolytic, but not in oxidative muscle. In PGC-1β KO mice, atorvastatin induced a shift from oxidative type IIA to glycolytic type IIB myofibers mainly in oxidative muscle and mitochondrial dysfunction was observed in both muscle types. In glycolytic muscle of WT and KO mice and in oxidative muscle of KO mice, atorvastatin suppressed mitochondrial proliferation and oxidative defense, leading to apoptosis. In contrast, mitochondrial function was maintained or improved and apoptosis decreased by atorvastatin in oxidative muscle of WT mice. In conclusion, PGC-1β has an important role in preventing damage to oxidative muscle in the presence of a mitochondrial toxicant such as atorvastatin.

scholarly journals Curcumin Improves Pulmonary Hypertension Rats by Regulating Mitochondrial Function

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Jing Chen ◽  
Wen Jiang ◽  
Fei Zhu ◽  
Qiong Wang ◽  
Haiyan Yang ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Mitochondrial Function ◽  
Vascular Remodeling ◽  
Control Group ◽  
Sprague Dawley ◽  
Pulmonary Vascular Remodeling ◽  
Sprague Dawley Rats ◽  
Pulmonary Arterial ◽  
Toxicological Mechanism ◽  
And Function

Objective. To investigate the role of curcumin in regulating pathogenesis of pulmonary arterial smooth muscle cells (PASMCs) derived from pulmonary arterial hypertension (PAH) model. Methods. Male Sprague Dawley rats were injected with monocrotaline (MCT) to establish the PAH experimental model. The rats were divided into control group, MCT group, and curcumin group. At the end of the study, hemodynamic data were measured to determine pulmonary hypertension. Proliferation ability of PASMCs, a remodeling indicator of pulmonary artery and right ventricle, was detected. In addition, the morphology and function of mitochondria, antiglycolysis and antiproliferation pathways, and genes were also analyzed. Results. Curcumin may function by reversing MCT-mediated pulmonary vascular remodeling in rats. Curcumin effectively improved pulmonary vascular remodeling, promoted PASMC apoptosis, and protected mitochondrial function. In addition, curcumin treatment suppressed the PI3K/AKT pathway in PASMCs and regulated the expression of antiproliferative genes. Conclusion. Curcumin can improve energy metabolism and reverse the process of PAHS. However, there were side effects of curcumin in MCT-induced rats, suggesting that the dosage should be treated with caution and its toxicological mechanism should be further studied and evaluated.

scholarly journals Pengaruh pemberian ekstrak pasak bumi (Eurycoma longifolia Jack) terhadap kualitas spermatozoa tikus wistar (Rattus norvegicus)

2016 ◽  
Vol 4 (1) ◽  
Author(s):  
Bill C. A. Bogar ◽  
Lydia Tendean ◽  
Grace L. A. Turalaki
Keyword(s):  
Rattus Norvegicus ◽  
Control Group ◽  
Adult Rats ◽  
Beneficial Effects ◽  
Eurycoma Longifolia ◽  
Male Wistar Rats ◽  
Group 3 ◽  
Eurycoma Longifolia Jack ◽  
Group 2 ◽  
Group 1

Abstract: Infertility is an inability of couples to reproduce after carrying out sexual intercourses for at least a year without using any contraceptives. There are 10-15% couples worldwide who experience infertility problems and almost one half of them is on men. Spermatozoa qualities including concentration, motility, and morphology are used as an indicator for men’s fertility. The utilization of herbal medicine (i.e. Eurycoma longifolia Jack extracts) is now being an alternative way to improve fertility among the community. This study was carried out to find the effects of Eurycoma longifolia Jack on spermatozoa qualities. This experimental study was conducted to nine male wistar rats (Rattus norvegicus) weighing from 200-250 grams, aging from 12-15 months. These nine adult rats were divided into 3 groups of 3 rats each. 400 and 600 mg/kg/day of Eurycoma longifolia Jack extracts were orally administrated to group 1 and 2 respectively, while group 3 were treated as control group. After 50 days, the animals of group 1, 2 and 3 were sacrificed. As a result, there is an improvement in qualities of spermatozoa which are statistically significant (p<0,05) in group 2. Thus, provide the beneficial effects of 600mg/kg Eurycoma longifolia Jack extracts on the qualities of spermatozoa.Keywords: pasak bumi, spermatozoaAbstrak: Infertilitas adalah ketidakmampuan pasangan untuk dapat hamil setelah satu tahun berhubungan intim tanpa menggunakan kontrasepsi. Ada sekitar 10 – 15 % pasangan mengalami masalah infertilitas dan hampir setengahnya masalah ada pada pria. Kualitas spermatozoa meliputi konsentrasi, motilitas dan morfologi spermatozoa merupakan salah satu indikator fertilitas pada pria. Penggunaan tanaman herbal atau yang lebih dikenal jamu telah menjadi pengobatan alternatif di masyarakat. Tanaman herbal yang dimaksud adalah pasak bumi. Penelitian ini bertujuan untuk mengetahui efek dari esktrak pasak bumi (Eurycoma longifolia Jack) terhadap kualitas spermatozoa. Penelitian ini menggunakan 9 ekor tikus wistar jantan (Rattus norvegicus) dengan berat badan 200-250 g berumur 12-15 bulan. Sembilan ekor wistar dibagi menjadi tiga kelompok, dan satu kelompok terdiri dari tiga ekor tikus wistar. Penelitian ini dilaksankan selama 50 hari. Esktrak pasak bumi (Eurycoma longifolia Jack) diberikan dengan dosis 400mg/kgBB per hari pada perlakuan 1 dan dosis 600 mg/kgBB per hari pada perlakuan 2. Setelah 50 hari hewan coba pada kelompok kontrol, perlakuan 1 dan perlakuan 2 diterminasi. Hasil penelitian memperlihatkan terjadi peningkatan kualitas spermatozoa yang signifikan secara statistik (p<0,05) pada perlakuan 2 terhadap kelompok kontrol. Hasil tersebut menunjukan bahwa Esktrak pasak bumi (Eurycoma longifolia Jack) pada dosis 600 mg/kgBB dapat meningkatkan kualitas spermatozoa.Kata kunci: pasak bumi, spermatozoa

scholarly journals Mitochondria-Cytokine Crosstalk Following Skeletal Muscle Injury and Disuse: A Mini-Review

2021 ◽  
Author(s):  
Anita E. Qualls ◽  
W. Michael Southern ◽  
Jarrod A. Call
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Function ◽  
Muscle Injury ◽  
Muscle Injuries ◽  
Monocyte Chemoattractant Protein 1 ◽  
Skeletal Muscle Injury ◽  
Atp Production ◽  
Bona Fide ◽  
Sense And Respond ◽  
And Function

Skeletal muscle mitochondria are highly adaptable, highly dynamic organelles that maintain the functional integrity of the muscle fiber by providing ATP for contraction and cellular homeostasis (e.g., Na+/K+ ATPase). Emerging as early modulators of inflammation, mitochondria sense and respond to cellular stress. Mitochondria communicate with the environment, in part, by release of physical signals called mitochondrial-derived damage-associated molecular patterns (mito-DAMPs) and deviation from routine function (e.g. reduced ATP production, Ca2+ overload). When skeletal muscle is compromised, mitochondria contribute to an acute inflammatory response necessary for myofibril regeneration; however, exhaustive signaling associated with altered or reduced mitochondrial function can be detrimental to muscle outcomes. Here we describe changes in mitochondrial content, structure, and function following skeletal muscle injury and disuse and highlight the influence of mitochondrial-cytokine crosstalk on muscle regeneration and recovery. While the appropriate therapeutic modulation following muscle stressors remains unknown, retrospective gene expression analysis reveal interleukin-6 (IL-6), interleukin-1b (IL-1b), chemokine C-X-C motif ligand 1 (CXCL1), and monocyte chemoattractant protein 1 (MCP-1) are significantly upregulated following three unique muscle injuries. These cytokines modulate mitochondrial function and execute bona fide pleiotropic roles that can aid functional recovery of muscle; however, when aberrant, chronically disrupt healing partly by exacerbating mitochondrial dysfunction. Multidisciplinary efforts to delineate the opposing regulatory roles of inflammatory cytokines in the muscle-mitochondrial environment are required to modulate regenerative behavior following skeletal muscle injury or disuse. Future therapeutic directions to consider include quenching or limited release of mito-DAMPs and cytokines present in cytosol or circulation.

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