Caffeine from four cups of coffee protects the heart with the help of mitochondria
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- Published on 26 July 2019
A new study shows that a caffeine concentration equivalent to four cups of coffee promotes the movement of a regulatory protein into mitochondria, enhancing their function and protecting cardiovascular cells from damage.
Caffeine consumption has been associated with lower risks for multiple diseases, including type II diabetes, heart disease, and stroke, but the mechanism underlying these protective effects has been unclear. A new study now shows that caffeine promotes the movement of a regulatory protein into mitochondria, enhancing their function and protecting cardiovascular cells from damage. The work, publishing 21 June in the open access journal PLOS Biology, by Judith Haendeler and Joachim Altschmied of the Medical Faculty, Heinrich-Heine-University and the IUF-Leibniz Research Institute for Environmental Medicine in Duesseldorf, Germany, and colleagues, found that the protective effect was reached at a concentration equivalent to consumption of four cups of coffee, suggesting the effect may be physiologically relevant.
News source: https://www.sciencedaily.com/releases/2018/06/180621141008.htm
PLOS. "Caffeine from four cups of coffee protects the heart with the help of mitochondria." ScienceDaily. ScienceDaily, 21 June 2018. <www.sciencedaily.com/releases/2018/06/180621141008.htm>.
Program of Targeting Mitochondria 2019 Congress/Speakers/Early Registration/May 21, 2019
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- Published on 15 May 2019
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Mitochondrial Copper Toxicity with a Focus on Wilson Disease
Selective segregation of mitochondria in asymmetric stem cell divisions
Cardiac glycosides modulate neuroblastoma stem cell survival by dysfunctional mitophagy
Mitochondria, as central regulators of neural stem cell fate
The cellular stress protein MNRR1/CHCHD2 and mitochondrial disease
Cannabinoids and skin: The "c(ut)annabinoid" system as a novel player in regulating cutaneous mitochondrial biology
Mitochondrial reactive oxygen species in heart failure
Biparental Inheritance of Mitochondrial DNA in Humans
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- Published on 10 December 2018
Photo Credit: seal1837, Pixabay
Significance
The energy-producing organelle mitochondrion contains its own compact genome, which is separate from the nuclear genome. In nearly all mammals, this mitochondrial genome is inherited exclusively from the mother, and transmission of paternal mitochondria or mitochondrial DNA (mtDNA) has not been convincingly demonstrated in humans. In this paper, we have uncovered multiple instances of biparental inheritance of mtDNA spanning three unrelated multiple generation families, a result confirmed by independent sequencing across multiple unrelated laboratories with different methodologies. Surprisingly, this pattern of inheritance appears to be determined in an autosomal dominantlike manner. This paper profoundly alters a widespread belief about mitochondrial inheritance and potentially opens a novel field in mitochondrial medicine.Abstract
Although there has been considerable debate about whether paternal mitochondrial DNA (mtDNA) transmission may coexist with maternal transmission of mtDNA, it is generally believed that mitochondria and mtDNA are exclusively maternally inherited in humans. Here, we identified three unrelated multigeneration families with a high level of mtDNA heteroplasmy (ranging from 24 to 76%) in a total of 17 individuals. Heteroplasmy of mtDNA was independently examined by high-depth whole mtDNA sequencing analysis in our research laboratory and in two Clinical Laboratory Improvement Amendments and College of American Pathologists-accredited laboratories using multiple approaches. A comprehensive exploration of mtDNA segregation in these families shows biparental mtDNA transmission with an autosomal dominantlike inheritance mode. Our results suggest that, although the central dogma of maternal inheritance of mtDNA remains valid, there are some exceptional cases where paternal mtDNA could be passed to the offspring. Elucidating the molecular mechanism for this unusual mode of inheritance will provide new insights into how mtDNA is passed on from parent to offspring and may even lead to the development of new avenues for the therapeutic treatment for pathogenic mtDNA transmission.
Reference: Shiyu Luo, C. Alexander Valencia, Jinglan Zhang, Ni-Chung Lee, Jesse Slone, Baoheng Gui et al. 2018. Biparental Inheritance of Mitochondrial DNA in Humans. PNAS. doi.org/10.1073/pnas.1810946115
News source: www.pnas.org
Marvin Edeas - A Pilot Study - Microbiota Quality and Mitochondrial Activity Link with Occurrence of Muscle Cramps ...
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- Published on 25 April 2019
Marvin Edeas explains Microbiota Quality and Mitochondrial Activity Link with Occurrence of Muscle Cramps in Hemodialysis Patients using Citrate Dialysate: A Pilot Study
Authors: Pierre-Yves Durand, Carole Nicco, Dedier Serteyn, David Attaf, Marvin Edeas
BACKGROUND/AIMS:
Hemodialysis-associated muscle cramp (HAMC) is a common complication under citrate dialysate (CD) occurring in 30% of cases. Our objectives were to assess the gut microbiota quality, mitochondrial activity, and to investigate their possible relationship with HAMC.
METHODS:
Ten end-stage renal disease patients (78.9 ± 2.1 years) treated by hemodialysis (HD) with CD were enrolled and then classified according to the frequency of HAMCs: "frequent HAMCs group" (n = 5) and "absence of HAMCs group" (n = 5). Gut microbiota quality, mitochondrial activity, and some markers of oxidative stress (OS) were investigated.
RESULTS:
In patients with cramps, gut microbiota diversity seemed lower and some genera including Helicobacter, Lachnospira, Roseburia, and Haemophilus seemed over-expressed, a significant increase of citratemia and significant lowering mitochondrial function were observed. No difference was observed on the OS markers.
CONCLUSION:
This first clinical study revealed a possible dysbiosis of microbiota and a mitochondrial dysfunction into HD patients with cramps under CD compared to patients without cramp.
© 2018 S. Karger AG, Basel.
New research reveals a mitochondrial gene that protects against dementia and other diseases of aging
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- Published on 28 September 2018
Image source: www.gero.usc.edu
New research from USC has uncovered a previously unknown genetic risk factor for Alzheimer’s disease and related dementias. The study provides insights on how these conditions, and other diseases of aging, might one day be treated and prevented.
The research from the Cohen Lab at the USC Leonard Davis School of Gerontology sheds new light on the protective role of a naturally occurring mitochondrial peptide, known as humanin. Amounts of the peptide decrease with age, leading researchers to believe that humanin levels play an important function in the aging process and the onset of diseases linked to older age.
“Because of the beneficial effects of humanin, a decrease in circulating levels could lead to an increase in several different diseases of aging, particularly in dementia,” said senior author Pinchas Cohen, dean of the USC Leonard Davis School and one of three researchers to independently discover the existence of humanin 15 years ago.
The study, Humanin Prevents Age-Related Cognitive Decline in Mice and is Associated with Improved Cognitive Age in Humans, led by Kelvin Yen of the USC Leonard Davis School, appears online on Sept. 21 in the Nature-published journal Scientific Reports. Among the findings, the researchers discovered a significant difference between the circulating levels of humanin in African-Americans, who are more impacted by Alzheimer’s disease and other diseases of aging, as compared to Caucasians.
“We have now discovered a novel underlying biological factor that may be contributing to this health disparity,” said Yen, a research assistant professor of gerontology.
Because humanin is encoded within the mitochondrial genome, the research team examined the mitochondrial DNA for common genetic variations known as SNPs (pronounced snips) that could explain the differences between humanin levels. According to the paper, after sequencing the entire mitochondrial genome of all samples to determine if any SNPs correlated with humanin levels, they identified a genetic variation that was associated with a 14 percent decrease in circulating humanin levels.
This provides the first evidence that a variation in the sequence of a mitochondrial peptide is associated with a change in the level of peptides and the first conclusive demonstration that mitochondrial peptides are encoded in and regulated through mitochondrial DNA, Cohen said.
The team subsequently examined the effect of this SNP in a separate large cohort of participants from the Health and Retirement Study, a longitudinal study of approximately 20,000 individuals over the age of 50 in the United States, of which more than 12,500 individuals consented to DNA analysis. Using this data set, the researchers report finding that the unfavorable version of this SNP, associated with low levels of the humanin peptide, is also associated with accelerated cognitive aging, providing the first demonstration linking a humanin SNP in the mitochondria to cognitive decline in people.
The paper also shows that in mice, injections of humanin delay cognitive decline associated with aging, proposing a possible therapeutic role for humanin-related drugs. The mechanism through which humanin acts to mediate these effects involves suppression of inflammation systemically, as well as specifically in the brain.
News source: www.gero.usc.edu
