Results 41 to 50 of about 5,164,021 (213)

Mitochondrial DNA deletions and neurodegeneration in multiple sclerosis [PDF]

open access: yes, 2010
Cerebral atrophy is a correlate of clinical progression in multiple sclerosis (MS). Mitochondria are now established to play a part in the pathogenesis of MS.
Turnbull, Doug M   +18 more
core   +1 more source

The Guanylyl Cyclase Activator YC-1 Directly Inhibits the Voltage-Dependent K+ Channels in Rabbit Coronary Arterial Smooth Muscle Cells

open access: yesJournal of Pharmacological Sciences, 2010
We investigated the effects of YC-1, an activator of soluble guanylyl cyclase (sGC), on voltage-dependent K+ (Kv) channels in smooth muscle cells from freshly isolated rabbit coronary arteries by using the whole-cell patch clamp technique. YC-1 inhibited
Won Sun Park   +9 more
doaj   +1 more source

Parkinson phenotype in aged PINK1-deficient mice is accompanied by progressive mitochondrial dysfunction in absence of neurodegeneration [PDF]

open access: yes, 2009
Background Parkinson's disease (PD) is an adult-onset movement disorder of largely unknown etiology. We have previously shown that loss-of-function mutations of the mitochondrial protein kinase PINK1 (PTEN induced putative kinase 1) cause the recessive ...
Rüb Udo   +107 more
core   +1 more source

Mitochondria, neurosteroids and biological rhythms : implications in health and disease states [PDF]

open access: yes, 2015
Mitochondria are considered as the “powerhouses” of cells because they synthesize the universal source of energy under the form of adenosine triphosphate (ATP) molecules via oxidative phosphorylation from nutritional sources. Thus, impaired mitochondrial
Grimm, Amandine
core   +1 more source

Quality Matters? The Involvement of Mitochondrial Quality Control in Cardiovascular Disease

open access: yesFrontiers in Cell and Developmental Biology, 2021
Cardiovascular diseases are one of the leading causes of death and global health problems worldwide. Multiple factors are known to affect the cardiovascular system from lifestyles, genes, underlying comorbidities, and age.
Kai-Lieh Lin   +18 more
doaj   +1 more source

Mitochondrial DNA mutations affect calcium handling in differentiated neurons. [PDF]

open access: yes, 2010
Contains fulltext : 88975.pdf (Publisher’s version ) (Closed access)Mutations in the mitochondrial genome are associated with a wide range of neurological symptoms, but many aspects of the basic neuronal pathology are not understood ...
Enriquez, J.A.   +26 more
core   +2 more sources

Gut microbiome and aging—A dynamic interplay of microbes, metabolites, and the immune system

open access: yesFEBS Letters, EarlyView.
Age‐dependent shifts in microbial communities engender shifts in microbial metabolite profiles. These in turn drive shifts in barrier surface permeability of the gut and brain and induce immune activation. When paired with preexisting age‐related chronic inflammation this increases the risk of neuroinflammation and neurodegenerative diseases.
Aaron Mehl, Eran Blacher
wiley   +1 more source

Deceleration of fusion–fission cycles improves mitochondrial quality control during aging [PDF]

open access: yes, 2012
Mitochondrial dynamics and mitophagy play a key role in ensuring mitochondrial quality control. Impairment thereof was proposed to be causative to neurodegenerative diseases, diabetes, and cancer.
Michael Meyer-Hermann   +18 more
core   +2 more sources

A Novel Atypical PKC-Iota Inhibitor, Echinochrome A, Enhances Cardiomyocyte Differentiation from Mouse Embryonic Stem Cells

open access: yesMarine Drugs, 2018
Echinochrome A (EchA) is a marine bioproduct extracted from sea urchins having antioxidant, antimicrobial, anti-inflammatory, and chelating effects, and is the active component of the clinical drug histochrome.
Hyoung Kyu Kim   +11 more
doaj   +1 more source

An isoform of 14‐3‐3 protein regulates transbilayer lipid movement at the plasma membrane

open access: yesFEBS Letters, EarlyView.
Loss of 14‐3‐3ζ in CHO cells confers resistance to exogenous phosphatidylserine (PS) and impairs endocytosis‐independent inward flip‐flop of fluorescent PS at the plasma membrane. RNAi‐mediated knockdown reproduces this defect, while no additive effect is seen in ATP11C‐deficient cells.
Akiko Yamaji‐Hasegawa   +3 more
wiley   +1 more source

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