743 results about "Mitophagy" patented technology

The invention provides a method and a device for detecting mutated proteins. The method includes acquiring transcriptome data corresponding to samples; comparing the transcriptome data to mitochondrion databases and outputting non-mitochondrion sequences according to comparison results of the transcriptome data and the mitochondrion databases; transforming nucleotide sequences in the non-mitochondrion sequences into amino acid sequences, comparing the transformed amino acid sequences to protein databases and extracting amino acid sequences with homogenous rates in first set ranges and amino acid lengths in second set ranges from comparison results of the transformed amino acid sequences and the protein databases; comparing the extracted amino acid sequences with the homogenous rates in the first set ranges and the amino acid lengths in the second set ranges to NCBI (national center of biotechnology information) and determining the mutated proteins according to comparison results of the extracted amino acid sequences and the NCBI. According to the scheme, the method and the device have the advantage that the mutated proteins in the samples can be detected by the aid of the method and the device.

The present invention relates to the use of individual fumaric acid derivatives or mixtures thereof for preparing a pharmaceutical composition for treating mitochondrial diseases, especially for treating Parkinson's syndrome, Alzheimer's disease, Chorea Huntington disease, retinopathia pigmentosa and mitochondrial encephalomyopathy. Preferably, the fumaric acid derivative(s) is / are those selected from the group consisting of fumaric acid dialkyl esters or fumaric acid monoalkyl esters in the form of the free acid or a salt thereof.

Compositions and methods useful for inducing an increase in fatty acid oxidation or mitochondrial biogenesis, reducing weight gain, inducing weight loss, or increasing Sirt1, Sirt3, or AMPK activity are provided herein. Such compositions can contain synergizing amounts of a sirtuin-pathway activators, including but not limited to resveratrol, in combination with beta-hydroxymethylbutyrate (HMB), keto isocaproic acid (KIC), leucine, or combinations of HMB, KIC and leucine.

The present invention relates to compositions and methods for providing mitochondria-selective targeting agents covalently linked to desired cargo such as radical scavenging agents. Compositions and methods are disclosed for treating an illness that is caused or associated with cellular damage or dysfunction which is caused by excessive mitochondrial production of reaction oxygen species (ROS). Compositions which act as mitochondria-selective targeting agents using specific structural signaling features recognizable by cells as mitochondrial targeting sequences are discussed. A method for delivering these agents effectively into cells and mitochondria where they act as electron scavengers by way of certain targeting sequences is also disclosed. Mitochondria and cell death by way of apoptosis is inhibited as a result of the ROS-scavenging activity, thereby increasing the survival rate of the patient. In a preferred embodiment, the compositions and methods may be administered therapeutically in the field to patients with profound hemorrhagic shock so that survival could be prolonged until it is feasible to obtain surgical control of the bleeding vessels. In further preferred embodiments, the composition for scavenging radicals in a mitochondrial membrane includes a radical scavenging agent and a membrane active compound having a high affinity with said mitochondrial membrane and associated methods. In another embodiment, the cargo transported by mitochondrial-selective targeting agents may include an inhibitor of nitrous oxide system (NOS) enzyme activity.

Compositions and methods are disclosed for treating an illness that is caused or associated with cellular damage or dysfunction which is caused by excessive mitochondrial production of reaction oxygen species (ROS). Compositions which act as mitochondria-selective targeting agents using specific structural signaling features recognizable by cells as mitochondrial targeting sequences are discussed. A method for delivering these agents effectively into cells and mitochondria where they act as electron scavengers by way of certain targeting sequences is also disclosed. Mitochondria dysfunction and cell death by way of apoptosis is inhibited as a result of the ROS-scavenging activity, thereby increasing the survival rate of the patient. In a preferred embodiment, the compositions and methods may be administered therapeutically in the field to patients with profound hemorrhagic shock so that survival could be prolonged until it is feasible to obtain surgical control of the bleeding vessels.

The present invention provides methods for rapid forensic analysis of mitochondrial DNA and methods for characterizing heteroplasmy of mitochondrial DNA, which can be used to assess the progression of mitochondrial diseases.

Compounds, compositions, and methods are provided for treatment of disorders related to mitochondrial dysfunction. The methods comprise administering to a mammal a composition containing pyrimidine nucleotide precursors in amounts sufficient to treat symptoms resulting from mitochondrial respiratory chain deficiencies.

The present invention discloses novel mechanisms in the aging process and describes novel methods for high-throughput screening to identify, detect, and purify agents to be used for improving mitochondrial function, maintaining the cell cycle-arrested state in senescent and post mitotic cells, and thus preventing or treating age-related diseases or disorders associated with accelerated mitochondrial function loss, telomere dysfunction, and / or deterioration of the growth-arrested state. The present invention also discloses a number of compounds or compositions identified from this method. The present invention further provides the use of low doses of rapamycin or its analogs as a mimic of caloric restriction in preventing age-related diseases or disorders.

A method of detecting presence or absence of prostate cancer in a subject, both in vivo and ex vivo is disclosed. The method comprises analyzing mitochondria or a mitochondrial component in at least one prostate cell of the subject, whereby mitochondria an alteration in quantity and or characteristic is indicative of the presence or absence of the prostate cancer in the subject.

Methods of treating mitochondrial disorders that are not respiratory chain disorders using compositions comprising EPO mimetic compounds or compounds capable of increasing endogenous EPO levels or stimulating erythropoiesis are disclosed. Methods of treating Friedreich's ataxia, Leigh's syndrome, or other disorders by increasing the expression of frataxin with an EPO mimetic compound or a compound capable of increasing endogenous EPO levels or stimulating erythropoiesis are also disclosed.

Methods for the reduction of mitochondrial oxidative damage and improved mitochondrial efficiency in an animal by administration of medium chain triglycerides or prodrug of medium chain triglycerides to the animal are provided.

Methods of treating mitochondrial respiratory chain disorders using compounds having erythropoietin activity or thrombopoietin activity are disclosed. Indicators for assessing the efficacy of treatment are discussed.

The present invention relates to improved diagnostic methods for early detection of a risk for developing an arthritic disorder in humans, and screening assays for therapeutic agents useful in the treatment of arthritic disorders, by comparing the levels of one or more indicators of altered mitochondrial function. Indicators of altered mitochondrial function include enzymes such as mitochondrial enzymes and ATP biosynthesis factors. Other indicators of altered mitochondrial function include mitochondrial mass, mitochondrial number and mitochondrial DNA content, cellular responses to elevated intracellular calcium and to apoptogens, and free radical production. Methods of treating, and of stratifying, human patients as such methods relate to disclosed indicators of altered mitchondrial function are also provided.

A method for preventing, reducing, ameliorating or treating ophthalmic disorders associated with neurodegenerative diseases or trauma, comprising the topical, periocular, or intraocular application of an ophthalmic formulation comprising a therapeutically effective amount of one or more ophthalmic agents selected from the group consisting of alpha-tocotrienol, beta-tocotrienol, gamma-tocotrienol, delta-tocotrienol, or esters or mixtures thereof is disclosed. Use of tocotrienols for the prevention, reduction, amelioration or treatment of ophthalmic disorders that are, or that are associated with, mitochondrial diseases is also discussed. Topical ophthalmic formulations comprising tocotrienols are also discussed.

Methods of treating, preventing or suppressing symptoms associated with mitochondrial diseases, such as Friedreich's ataxia (FRDA), Leber's Hereditary Optic Neuropathy (LHON), dominant optic atrophy (DOA); mitochondrial myopathy, encephalopathy, lactacidosis, stroke (MELAS), Leigh syndrome or Kearns-Sayre Syndrome (KSS) with vitamin K are disclosed.

Compositions and methods are disclosed for treating an illness that is caused or associated with cellular damage or dysfunction which is caused by excessive mitochondrial production of reaction oxygen species (ROS). Compositions which act as mitochondria-selective targeting agents using specific structural signaling features recognizable by cells as mitochondrial targeting sequences are discussed. A method for delivering these agents effectively into cells and mitochondria where they act as electron scavengers by way of certain targeting sequences is also disclosed. Mitochondria dysfunction and cell death by way of apoptosis is inhibited as a result of the ROS-scavenging activity, thereby increasing the survival rate of the patient. In a preferred embodiment, the compositions and methods may be administered therapeutically in the field to patients with profound hemorrhagic shock so that survival could be prolonged until it is feasible to obtain surgical control of the bleeding vessels.

Disclosed herein are phenazine-3-one and phenothiazine-3-one derivative compounds and methods of using such compounds for treating or suppressing oxidative stress disorders, including mitochondrial disorders, impaired energy processing disorders, neurodegenerative diseases and diseases of aging.

The present invention provides methods of using electromagnetic radiation in the visible portion of the spectrum to modulate mitochondrial function in the treatment of various conditions, including Alzheimer's disease, other dementias, hypoxia and diabetic peripheral neuropathy, and sensory disorders of the extremities.

The invention relates the method of treatment or amelioration of mitochondrial disorders such as Alzheimer's disease, Parkinson's disease, Friedreich's ataxia (FRDA), cerebellar ataxias, Leber's hereditary optic neuropathy (LHON), mitochondrial myopathy, encephalopathy, lactacidosis, stroke (MELAS), Myoclonic Epilepsy with Ragged Red Fibers (MERFF), amyotrophic lateral sclerosis (ALS), motor neuron diseases, Huntington's disease, macular degeneration, and epilepsy, with chroman derivatives of Formula I or Formula II as described herein.

The present invention provides methods of using electromagnetic radiation in the visible portion of the spectrum to modulate mitochondrial function in the treatment of various conditions, including Alzheimer's disease, other demential, hypoxia and diabetic peripheral neuropathy, and sensory disorders of the extremities.

The present invention relates to methods and formulations for the prevention or treatment of diseases or conditions associated with oxidative stress, inflammation, and metabolic dysregulation. Specifically, the present invention comprises compositions and methods that increase mitochondrial biogenesis, alleviate inflammation, and increase the level of endogenous enzymatic and non-enzymatic antioxidants in a subject.

Provided herein are methods and compositions for treating or preventing metabolic disorders, such as obesity and diabetes. Methods may comprise modulating the activity or level of a sirtuin, such as SIRTl or Sir2. Exemplary methods comprise contacting a cell with a sirtuin activating compound, such as a flavone, stilbene, flavanone, isoflavone, catechin, chalcone, tannin or anthocyanidin, or an inhibitory compound, such as nicotinamide.

Methods and compositions comprising peroxisomal and / or mitochondrial beta oxidation stimulating agents to reverse or resolve, slow the progression of, treat or prevent the development of fatty liver and conditions stemming from fatty liver, such as NASH, liver inflammation, cirrhosis and liver failure. An active agent that by itself is associated with an increased risk of fatty liver development and conditions stemming from fatty liver, such as NASH, liver inflammation, cirrhosis and liver failure, may be administered in combination with peroxisomal and / or mitochondrial beta oxidation stimulating agents. A combination regimen involving such agents, as simultaneous or concomitant therapy, or as a fixed dosage form, is also provided.

The invention provides a method and a kit using a mito-CRISPR / Cas9 system for editing DNA of abnormal mitochondria. The kit comprises DNA fragments for human or fish mitochondria, targeting mitochondrion gRNA and a mito-CRISPR / Cas9 expression system. The mito-CRISPR / Cas9 system comprises mitochondrial localization signal mNLS and mCas 9 protein or mRNA and correlated expression vector of mCas 9. The mito-CRISPR / Cas9 system is used for targeting deletion of DNA of the abnormal mitochondria in human and fish cells, so that proportion of normal mitochondria is increased, normal mitochondria are dominant, and mitochondrial diseases are treated by correcting mutation sites.

The present invention provides a mitochondrial activator containing pyrroloquinoline quinone, preferably pyrroloquinoline quinone and coenzyme Q (particularly reduced coenzyme Q) as active ingredients. In addition, the present invention provides a mitochondrial activator containing citric acid, preferably citric acid and coenzyme Q (particularly reduced coenzyme Q), as active ingredients. Since pyrroloquinoline quinone or citric acid exhibits a synergistic mitochondria activating effect with coenzyme Q (particularly reduced coenzyme Q), a high effect can be obtained even at a low dose. According to the present invention, therefore, a safer and practical mitochondrial activator is provided. The present invention further provides an agent for the prophylaxis or treatment of a disease caused by mitochondrial dysfunction.

The invention discloses a CRISPR / Cpf1 gene editing method applicable to a marine crustacean mitochondrion genome. The method includes the steps: introducing MLS signals positioned by a marine crustacean mitochondrion into a CRISPR / Cpf1 expression plasmid; designing gRNA; micro-injecting fertilized eggs; culturing the fertilized eggs in an in-vitro manner; detecting editing effect to complete editing of the marine crustacean mitochondrion genome. By the method, the marine crustacean mitochondrion genome can be directionally edited, and the method has significant value to a condition that artificial proliferation releasing markers are introduced into the marine crustacean mitochondrion genome.

This invention discloses methods of using krill oil and compositions comprising krill oil to treat risk factors for metabolic, cardiovascular, and inflammatory disorders. The present invention also relates to methods of using compositions comprising krill oil to modulate biological processes selected from the group consisting of glucose metabolism, lipid biosynthesis, fatty acid metabolism, cholesterol biosynthesis, and the mitochondrial respiratory chain. The present invention further includes pharmaceutical and / or nutraceutical formulations made from krill oil, methods of making such formulations, and methods of administering them to treat risk factors for metabolic, cardiovascular, and inflammatory disorders.

The embodiment of the invention discloses a universal primer mixture for animal mitochondria genome amplification as well as a design and amplification method thereof, and a kit comprising the universal primer mixture. By utilizing the primer mixture or the kit and the animal mitochondria genome amplified method and combining the novel high throughput sequencing technique, the animal mitochondria genome information can be efficiently obtained in low cost.

Compositions and methods useful for inducing an increase in fatty acid oxidation or mitochondrial biogenesis, reducing weight gain, inducing weight loss, or increasing Sirt1, Sirt3, or AMPK activity are provided herein. Such compositions can contain synergizing amounts of a sirtuin-pathway activators, including but not limited to resveratrol, in combination with beta-hydroxymethylbutyrate (HMB), keto isocaproic acid (KIC), leucine, or combinations of HMB, KIC and leucine.