Cellular and Molecular Life Sciences, Journal Year: 2021, Volume and Issue: 78(8), P. 3969 - 3986
Published: Feb. 12, 2021
Language: Английский
Biomolecules, Journal Year: 2020, Volume and Issue: 10(1), P. 85 - 85
Published: Jan. 5, 2020
Mitochondria are key regulators of cell fate through controlling ATP generation and releasing pro-apoptotic factors. Cardiac ischemia/reperfusion (I/R) injury to the coronary microcirculation has manifestations ranging in severity from reversible edema interstitial hemorrhage. A number mechanisms have been proposed explain cardiac microvascular I/R including edema, impaired vasomotion, microembolization, capillary destruction. In contrast their role types with higher energy demands, mitochondria endothelial cells primarily function signaling cellular responses environmental cues. It is clear that abnormal mitochondrial signatures, oxidative stress, fission, fusion, mitophagy, play a substantial function. While pathogenic each these alterations remains complex, profiling stress dynamics dysfunction may offer promising potential targets search for novel diagnostics therapeutics injury. The objective this review discuss on dysfunction. Mitochondrial dynamics, fission critically discussed understand roles survival. Finally, as degradative mechanism damaged mitochondria, summarized figure out its contribution progression
Language: Английский
Citations
103
Frontiers in Physiology, Journal Year: 2020, Volume and Issue: 11
Published: Feb. 14, 2020
Doxorubicin is a valuable antineoplastic drug although its clinical use greatly hindered by severe cardiotoxicity with dismal target therapy available. Luteolin natural product extracted from vegetables and fruits wide range of biological efficacies including anti-oxidative, anti-tumorigenic, anti-inflammatory properties. This study was designed to examine the possible effect luteolin on doxorubicin-induced cardiotoxicity, if any, mechanism(s) involved focus mitochondrial autophagy. application (10 μM) in adult mouse cardiomyocytes overtly improved cardiomyocyte contractile dysfunction elevated peak shortening amplitude maximal velocity shortening/relengthening along unchanged duration relengthening. alleviated apoptosis, accumulation reactive oxygen species (ROS) loss membrane potential. Furthermore, attenuated through promoting autophagy association facilitating phosphorylation Drp1 at Ser616, upregulating TFEB expression. In addition, treatment partially low dose elongation mitochondria. Treatment Mdivi-1, GTPase inhibitor, negated protective levels TFEB, LAMP1, LC3B, as well potential face doxorubicin challenge. Taken together, these findings provide novel insights for therapeutic efficacy against possibly
Language: Английский
Citations
95
Free Radical Biology and Medicine, Journal Year: 2023, Volume and Issue: 208, P. 236 - 251
Published: Aug. 9, 2023
Language: Английский
Citations
35
Biomedicine & Pharmacotherapy, Journal Year: 2018, Volume and Issue: 111, P. 151 - 161
Published: Dec. 19, 2018
Promoting epidermal cell survival in an oxidative stress microenvironment is vital for skin regeneration after burns and/or wounds. However, few studies have explored the mediators related to apoptosis microenvironment. Cellular viability was determined using MTT assay, TUNEL staining, western blot analysis and LDH release assay. Two independent siRNAs were transfected into HaCaT repress INF2 HIF1 presence of H2O2. Mitochondrial function JC-1 mitochondrial ROS immunofluorescence staining blotting. In present study, our data demonstrated that expression inverted formin-2 (INF2) increased rapidly when cells exposed Interestingly, knockdown promoted via reducing H2O2-mediated apoptosis. Molecular investigations deletion attenuated overloading, restored cellular redox balance, sustained membrane potential, improved respiratory corrected dynamics disorder H2O2-mimicking addition, upregulated HIF1. inhibition death caused despite INF2, suggesting signaling pathway required deletion-mediated protection. Altogether, results identified as a novel apoptotic mediator stress-mediated modulating repressing pathway. This finding provides evidence support critical role played by INF2-HIF1 axis regulating
Language: Английский
Citations
76
Free Radical Biology and Medicine, Journal Year: 2019, Volume and Issue: 135, P. 182 - 197
Published: March 5, 2019
Language: Английский
Citations
76
Redox Biology, Journal Year: 2019, Volume and Issue: 26, P. 101287 - 101287
Published: July 27, 2019
The basic pathophysiological mechanisms underlying septic cardiomyopathy have not yet been completely clarified. Disease-specific treatments are lacking, and care is still based on supportive modalities. aim of our study was to assess the protective effects melatonin cardiomyopathy, with a focus interactions between receptor-interacting protein kinase 3 (Ripk3), mitochondria, endoplasmic reticulum (ER) cytoskeletal degradation in cardiomyocytes. Ripk3 expression increased heart samples challenged LPS, followed by myocardial inflammation, cardiac dysfunction, breakdown cardiomyocyte death. treatment attenuated injury comparable manner genetic depletion Ripk3. Molecular investigations revealed that intimately regulated mitochondrial function, ER stress, homeostasis cardioprotective signaling pathways. Melatonin-mediated inhibition improved bioenergetics, reduced mitochondria-initiated oxidative damage, sustained dynamics, ameliorated normalized calcium recycling, activated pathways (including AKT, ERK AMPK) Interestingly, overexpression mediated resistance therapy following infection LPS-treated hearts an adenovirus expressing Altogether, findings identify upregulation as novel risk factor for development sepsis-related injury, restores physiological functions ER, contractile cytoskeleton Additionally, data also reveal new, potentially therapeutic mechanism which protects from sepsis-mediated possibly targeting
Language: Английский
Citations
72
Frontiers in Physiology, Journal Year: 2020, Volume and Issue: 11
Published: April 29, 2020
Melatonin is a pleiotropic, indole secreted and synthesized by the human pineal gland. has biological effects including anti-apoptosis, protecting mitochondria, anti-oxidation, anti-inflammation, stimulating target cells to secrete cytokines. Its protective effect on cardiomyocytes in acute myocardial infarction (AMI) caused widespread interest actions of this molecule. The melatonin against oxidative stress, promoting autophagic repair cells, regulating immune inflammatory responses, enhancing mitochondrial function, relieving endoplasmic reticulum play crucial roles from infarction. Mitochondrial apoptosis dysfunction are common occurrence cardiomyocyte injury after This review focuses targets infarction, main molecular signaling pathways that influences its endogenous role developmental prospect treatment.
Language: Английский
Citations
68
Cell Stress and Chaperones, Journal Year: 2019, Volume and Issue: 24(3), P. 595 - 608
Published: April 16, 2019
Irisin plays a protective effect in acute and chronic myocardial damage, but its role septic cardiomyopathy is unclear. The aim of our study was to explore the vivo vitro effects irisin using an LPS-induced model. Our results demonstrated that treatment attenuated LPS-mediated cardiomyocyte death dysfunction. At molecular level, LPS application associated with mitochondrial oxidative injury, ATP depletion caspase-related apoptosis activation. In contrast, sustained function by inhibiting DRP1-related fission reactivation impaired action on inflammation-attacked mitochondria cardiomyocytes. Additionally, we found modulated through JNK-LATS2 signaling pathway. JNK activation and/or LATS2 overexpression abolished beneficial stress death. Altogether, illustrate pathway participates pathogenesis cardiomyopathy. could be used future as effective therapy for sepsis-induced depression because it corrects normalizes
Language: Английский
Citations
55
International Journal of Biological Sciences, Journal Year: 2022, Volume and Issue: 18(14), P. 5276 - 5290
Published: Jan. 1, 2022
In diabetic cardiomyopathy (DCM), a major complication, the myocardium is structurally and functionally altered without evidence of coronary artery disease, hypertension or valvular disease.Although numerous anti-diabetic drugs have been applied clinically, specific medicines to prevent DCM progression are unavailable, so prognosis remains poor.Mitochondrial ATP production maintains energetic requirements cardiomyocytes, whereas mitochondrial dysfunction can induce aggravate by promoting oxidative stress, dysregulated calcium homeostasis, metabolic reprogramming, abnormal intracellular signaling apoptosis in cardiomyocytes.In response dysfunction, quality control (MQC) system (including fission, fusion, mitophagy) activated repair damaged mitochondria.Physiological fission fragments network isolate mitochondria.Mitophagy then allows dysfunctional mitochondria be engulfed autophagosomes degraded lysosomes.However, MQC results excessive impaired fusion delayed mitophagy, causing fragmented accumulate this review, we summarize molecular mechanisms discuss how pathological contributes development.We present promising therapeutic approaches improve progression.
Language: Английский
Citations
36
Cardiology Research and Practice, Journal Year: 2019, Volume and Issue: 2019, P. 1 - 16
Published: May 28, 2019
Worldwide morbidity and mortality from acute myocardial infarction (AMI) related heart failure remain high. While effective early reperfusion of the criminal coronary artery after a confirmed AMI is typical treatment at present, collateral ischemia-reperfusion injury (MIRI) pertinent cardioprotection are still challenging to address have inadequately understood mechanisms. Therefore, unveiling novel molecular targets networks participating in triggering resisting pathobiology MIRI promising valuable frontier. The present study specifically focuses on recent advances that supported by sophisticated bio-methodology order bring poorly interrelationship among pro- anti-MIRI participant molecules up date, as well identify findings may facilitate further investigation targets.
Language: Английский
Citations
52