Age and Sex Influence Mitochondria and Cardiac Health in Offspring Exposed to Maternal Glucolipotoxicity
Open accessAbstract
Infants of diabetic mothers are at risk of cardiomyopathy at birth and myocardial infarction in adulthood, but prevention is hindered because mechanisms remain unknown. We previously showed that maternal glucolipotoxicity increases the risk of cardiomyopathy and mortality in newborn rats through fuel-mediated mitochondrial dysfunction. Here we demonstrate ongoing cardiometabolic consequences by cross-fostering and following echocardiography, cardiomyocyte bioenergetics, mitochondria-mediated turnover, and cell death following metabolic stress in aged adults. Like humans, cardiac function improves by weaning with no apparent differences in early adulthood but declines again in aged diabetes-exposed offspring. This is preceded by impaired oxidative phosphorylation, exaggerated age-related increase in mitochondrial number, and higher oxygen consumption. Prenatally exposed male cardiomyocytes have more mitolysosomes indicating high baseline turnover; when exposed to metabolic stress, mitophagy cannot increase and cardiomyocytes have faster mitochondrial membrane potential loss and mitochondria-mediated cell death. Details highlight age- and sex-specific roles of mitochondria in developmentally programmed adult heart disease.
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Basal respiration in permeabilized cardiomyocytes from neonatal and 12-month-old offspring in the high-fat diet and STZ-induced diabetes model is similar.
“While basal respiration in permeabilized cardiomyocytes from neonatal and 12-month-old offspring were similar, altered state 3 respiration was apparent in mitochondria from 12-month-old offspring, particularly when using complex I fuels as substrates [111].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
The Results section on permeabilized cardiomyocytes (page unavailable) reports differences in basal oxygen consumption at 12 months: it is higher in diet-exposed females and lower in diabetes-exposed males. It does not support a blanket statement that basal respiration is similar in neonatal and 12-month-old offspring; the Results also report a 70-fold developmental increase in basal respiration in control cardiomyocytes. (LLM, conf=0.78)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredIn rat offspring of high-fat diet and STZ-induced diabetes dams aged up to 12 months, LV hypertrophy was not observed compared to controls.
“While LV hypertrophy was not observed in these offspring compared to controls, female offspring exhibited some systolic dysfunction (e.g., reduced ejection fraction) without diastolic dysfunction [111].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
The Results section on cardiac mass (page unavailable) reports larger heart-to-body-weight ratios at birth, particularly in offspring exposed to both maternal high-fat diet and diabetes. It also reports significantly larger ratios in diet-exposed males at 12 months and says left ventricular mass followed a similar pattern. These findings contradict the unqualified claim that LV hypertrophy was not observed through 12 months. (LLM, conf=0.85)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredMaternal diabetes does not affect LV mass in 12-month-old offspring.
“However, maternal diabetes did not affect the LV mass in 12-month-old offspring, though sex-specific effects on cardiac function were observed [111].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
The Results section on cardiac mass and function reports sex-specific functional effects at 12 months: diabetes-exposed females had poorer systolic function and males poorer diastolic function. It does not explicitly say that maternal diabetes had no effect on LV mass at that age; it says LV mass followed a pattern similar to heart mass, which changed differently by sex and exposure. Page numbers were not available in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measuredIn the combined maternal obesity and late-gestation streptozotocin model, body weights as well as serum glucose and triacylglycerol levels were similar to the respective male and female offspring of controls.
“Using this model, body weights as well as serum glucose and triacylglycerol levels were similar to the respective male and female offspring of controls [111].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
The Results section, “Metabolic Syndrome Does Not Explain Cardiac Disease,” reports similar weights across groups at 10 weeks and 6 months and similar circulating lipids at 3 weeks. But it also reports higher blood glucose in combination-exposed newborns and transiently higher triglycerides in exposed offspring at 10 weeks. Thus, the unqualified claim that all three measures were similar to controls is too broad. Page numbers are unavailable in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredMale offspring of diabetic dams exhibit reduced diastolic function without systolic impairments compared to controls.
“Male offspring exhibited reduced diastolic function without systolic impairments, while female offspring exhibited systolic dysfunction, but not diastolic dysfunction, compared to controls [111].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
The Results section on cardiac function reports that at 12 months, diabetes-exposed males had poorer diastolic function, while females had poorer systolic function. The claim omits that age qualifier: the same section reports poorer systolic and diastolic function in exposed newborns, with maternal diabetes particularly affecting systolic function in males. (LLM, conf=0.86)
Experimental — accuracy not yet measured
Impaired glucose oxidation observed in neonatal cardiomyocytes from the high-fat diet and STZ-induced diabetes model is attenuated by 10 weeks of age.
“Impaired glucose oxidation that was observed in neonatal cardiomyocytes was attenuated by 10 weeks of age, although reduced respiratory capacity re-emerges in cardiomyocytes at 6 months of age and is present in the cardiomyocytes from 12 months old offspring.”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
The Results section on cellular bioenergetics reports impaired neonatal respiratory capacity in diabetes- and high-fat-diet-exposed cardiomyocytes, with no group differences remaining by 10 weeks. It also reports impaired aerobic glycolysis in diabetes-exposed neonatal cells, but does not establish that the respiratory impairment in both exposure groups was specifically impaired glucose oxidation; the respiratory assay included both glucose and pyruvate. (LLM, conf=0.82)
Experimental — accuracy not yet measuredIn permeabilized cardiomyocytes from offspring of STZ-induced diabetes dams, lower basal respiration is observed.
“Mitochondrial respiration was examined in permeabilized cardiomyocytes and lower basal respiration was observed, but also a higher response to a complex IV substrate, indicating a lower flow of electrons through complexes I-III, but the ability to directly oxidize complex IV substrates, which requires more oxygen [111].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
The Results section on fuel-specific complex function (Figure 5; page unavailable) reports lower basal oxygen consumption and a higher response to a complex IV substrate in permeabilized cardiomyocytes from diabetes-exposed offspring. The finding is specifically for 12-month-old males, not offspring generally, and the paper says the proposed explanation about electron flow through complexes I–III *may* apply rather than stating it as established. (LLM, conf=0.88)
Experimental — accuracy not yet measuredFemale offspring of diabetic dams exhibit systolic dysfunction but not diastolic dysfunction compared to controls.
“Male offspring exhibited reduced diastolic function without systolic impairments, while female offspring exhibited systolic dysfunction, but not diastolic dysfunction, compared to controls [111].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
The Results section on cardiac function (page not provided) reports poorer systolic function in diabetes-exposed female offspring at 12 months, while reporting poorer diastolic function in males. The claim omits that age qualifier: the same section says both systolic and diastolic function were poorer in exposed offspring at birth, so the absence of diastolic dysfunction should not be stated generally. (LLM, conf=0.86)
Experimental — accuracy not yet measuredAltered state 3 respiration is apparent in mitochondria from 12-month-old offspring in the high-fat diet and STZ-induced diabetes model, particularly when using complex I fuels as substrates.
“While basal respiration in permeabilized cardiomyocytes from neonatal and 12-month-old offspring were similar, altered state 3 respiration was apparent in mitochondria from 12-month-old offspring, particularly when using complex I fuels as substrates [111].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
The Results section on complex function (Figure 5C, p. not available) reports altered fuel-stimulated state 3 respiration at 12 months, including lower responses to complex I fuels in diet-exposed females. The effects are sex- and exposure-specific, however, and the same section reports basal respiration differences at 12 months; it does not support the citing sentence’s unqualified statement that basal respiration was similar. (LLM, conf=0.85)
Experimental — accuracy not yet measuredIn permeabilized cardiomyocytes from offspring of STZ-induced diabetes dams, a higher response to a complex IV substrate is observed.
“Mitochondrial respiration was examined in permeabilized cardiomyocytes and lower basal respiration was observed, but also a higher response to a complex IV substrate, indicating a lower flow of electrons through complexes I-III, but the ability to directly oxidize complex IV substrates, which requires more oxygen [111].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
The Results section reports a higher response to the complex IV substrate TMPD-ascorbate in permeabilized cardiomyocytes from diabetes-exposed males at 12 months. The claim omits that age-and-sex restriction, making the finding sound applicable to offspring generally. The Results also describe the maternal diabetes model as streptozocin-induced. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThese offspring from a high-fat diet and diabetes during pregnancy also have higher baseline levels of mitolysosomes.
“These offspring also have higher baseline levels of mitolysosomes [111].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
The Results section, “Fetal Exposure and Sex Influence Physiologic Mitophagy in Aged Offspring CM” (page not provided), reports more baseline mitolysosomes in cardiomyocytes from diabetes-exposed offspring, particularly males, with the effect most apparent in combination-exposed males. It does not establish higher levels for all offspring exposed to both diabetes and a high-fat diet; diet-exposed cardiomyocytes had the lowest baseline levels. The measurements were in cardiomyocytes from 12-month-old offspring. (LLM, conf=0.87)
Experimental — accuracy not yet measuredFemale offspring of high-fat diet and STZ-induced diabetes dams exhibited some systolic dysfunction (e.g., reduced ejection fraction) without diastolic dysfunction.
“While LV hypertrophy was not observed in these offspring compared to controls, female offspring exhibited some systolic dysfunction (e.g., reduced ejection fraction) without diastolic dysfunction [111].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
The Results section on cardiac mass and function (page unavailable) reports poorer systolic function in 12-month-old diabetes-exposed females, but not diet-exposed females. It does not establish that females exposed to both maternal high-fat diet and diabetes had systolic dysfunction without diastolic dysfunction: at birth, diastolic function was poorer in diet-exposed offspring, especially females, and combination-exposed newborns had the poorest function. (LLM, conf=0.86)
Experimental — accuracy not yet measuredMale offspring of high-fat diet and STZ-induced diabetes dams had only diastolic dysfunction (e.g., reduced E/A ratio) and no difference in systolic function.
“In contrast, the male offspring had only diastolic dysfunction (e.g., reduced E/A ratio) and no difference in systolic function.”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
The Results section on cardiac function reports poorer diastolic function in exposed males at 12 months and identifies E:A ratio as its measure; it reports poorer systolic function at that age in females, not males. But the claim omits the age qualifier: the same section reports impaired systolic function in exposed newborn males, so 'only diastolic dysfunction' does not hold across ages. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThere is a lower flow of electrons through complexes I-III in cardiomyocytes from offspring of STZ-induced diabetes dams.
“Mitochondrial respiration was examined in permeabilized cardiomyocytes and lower basal respiration was observed, but also a higher response to a complex IV substrate, indicating a lower flow of electrons through complexes I-III, but the ability to directly oxidize complex IV substrates, which requires more oxygen [111].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
The Results section reports lower basal oxygen consumption and a higher response to a complex IV substrate in diabetes-exposed male cardiomyocytes, and says this may reflect lower electron flow through complexes I–III. The claim omits the male-specific finding and presents the proposed explanation as an established result. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMaternal high-fat diet feeding increased the heart weight:body weight ratio at 12 months of age in male, but not female offspring.
“However, Louwagie et al. [111] found that maternal high-fat diet feeding increased the heart weight:body weight ratio at 12 months of age in male, but not female offspring.”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
Maternal high-fat feeding had no effect on systolic or diastolic function of the heart in 12-month-old male and female offspring.
“A separate publication has shown that maternal high-fat feeding had no effect on systolic or diastolic function of the heart in 12-month-old male and female offspring [111].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
Mitochondria dysfunction is a key feature in the offspring heart in the high-fat diet and STZ-induced diabetes model.
“Despite increased mitochondrial DNA copy numbers in this model [111], these authors found that mitochondria dysfunction was a key feature in the offspring heart.”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
Maternal diabetes has sex-specific effects on cardiac function in 12-month-old offspring.
“However, maternal diabetes did not affect the LV mass in 12-month-old offspring, though sex-specific effects on cardiac function were observed [111].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
Female offspring in the high-fat diet and STZ-induced diabetes model had increased protein expression of NDUFA2 (complex I) in the heart.
“No differences in mitochondrial complex expression were observed in 12-month-old male offspring hearts, but females had increased protein expression of NDUFA2 (complex I).”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
Reduced palmitate oxidation is apparent in neonatal cardiomyocytes from the high-fat diet and STZ-induced diabetes model.
“In addition, reduced palmitate oxidation and glycolysis were apparent in the neonatal cardiomyocytes.”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
No differences in mitochondrial complex expression are observed in 12-month-old male offspring hearts in the high-fat diet and STZ-induced diabetes model.
“No differences in mitochondrial complex expression were observed in 12-month-old male offspring hearts, but females had increased protein expression of NDUFA2 (complex I).”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
Reduced glycolysis is apparent in neonatal cardiomyocytes from the high-fat diet and STZ-induced diabetes model.
“In addition, reduced palmitate oxidation and glycolysis were apparent in the neonatal cardiomyocytes.”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
Reduced respiratory capacity re-emerges in cardiomyocytes at 6 months of age and is present in cardiomyocytes from 12-month-old offspring in the high-fat diet and STZ-induced diabetes model.
“Impaired glucose oxidation that was observed in neonatal cardiomyocytes was attenuated by 10 weeks of age, although reduced respiratory capacity re-emerges in cardiomyocytes at 6 months of age and is present in the cardiomyocytes from 12 months old offspring.”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
Mitochondrial DNA copy numbers are increased in the high-fat diet and STZ-induced diabetes model.
“Despite increased mitochondrial DNA copy numbers in this model [111], these authors found that mitochondria dysfunction was a key feature in the offspring heart.”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
Baseline levels of mitolysosomes are elevated in offspring of STZ-induced diabetes dams.
“Baseline levels of mitolysosomes were also elevated [111].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
Morphologically, mitochondria in these offspring from a high-fat diet and diabetes during pregnancy were shorter, wider and more fragmented.
“Morphologically, these mitochondria were shorter, wider and more fragmented.”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [111]
The Results section on mitochondrial dynamism reports changes in fission- and fusion-related proteins, and the mitophagy Results report differences in mitochondrial clearance. Neither gives measurements showing that offspring mitochondria were shorter, wider, or more fragmented. Searches for those shape descriptions found no supporting passage in our copy. (LLM, conf=0.72)
Experimental — accuracy not yet measured
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Cites
Galluzzi, L., Vitale, I., Aaronson, S. A., Abrams, J. M., Adam, D., Agostinis, P., Alnemri, E. S., Altucci, L., Amelio, I., Andrews, D. W., et al. (2018) · Cell Death & Differentiation · doi:10.1038/s41418-017-0012-4 · Cited by 6,680 · see citing works
Heidenreich, P. A., Trogdon, J. G., Khavjou, O. A., Butler, J., Dracup, K., Ezekowitz, M. D., Finkelstein, E. A., Hong, Y., Johnston, S. C., Khera, A., et al. (2011) · Circulation · doi:10.1161/cir.0b013e31820a55f5 · Cited by 3,208 · see citing works
Mitophagy and Quality Control Mechanisms in Mitochondrial Maintenance
Pickles, S., Vigié, P., & Youle, R. J. (2018) · Current Biology · doi:10.1016/j.cub.2018.01.004 · Cited by 2,081 · see citing works
Banting lecture 1980: of pregnancy and progeny.
Freinkel, N. (1980) · Diabetes · doi:10.2337/diab.29.12.1023 · Cited by 1,366 · see citing works
Molecular mechanisms of diabetic cardiomyopathy
Bugger, H., & Abel, E. D. (2014) · Diabetologia · doi:10.1007/s00125-014-3171-6 · Cited by 903 · see citing works
Kubli, D. A., & Gustafsson, Å. B. (2012) · Circulation Research · doi:10.1161/circresaha.112.265819 · Cited by 792 · see citing works
Sacks, D. A., Hadden, D. R., Maresh, M., Deerochanawong, C., Dyer, A. R., Metzger, B. E., Lowe, L. P., Coustan, D. R., Hod, M., Oats, J. J. N., et al. (2012) · Diabetes Care · doi:10.2337/dc11-1641 · Cited by 687 · see citing works
Lopaschuk, G. D., & Jaswal, J. S. (2010) · Journal of Cardiovascular Pharmacology · doi:10.1097/fjc.0b013e3181e74a14 · Cited by 636 · see citing works
The mitochondrial permeability transition initiates autophagy in rat hepatocytes
Elmore, S. P., Qian, T., Grissom, S. F., & Lemasters, J. J. (2001) · The FASEB Journal · doi:10.1096/fj.01-0206fje · Cited by 607 · see citing works
Lipid Metabolism and Toxicity in the Heart
Goldberg, I. J., Trent, C. M., & Schulze, P. C. (2012) · Cell Metabolism · doi:10.1016/j.cmet.2012.04.006 · Cited by 586 · see citing works
(2013) · Obstetrics and Gynecology · doi:10.1097/01.aog.0000433006.09219.f1 · Cited by 583 · see citing works
Reynolds, R. M., Allan, K. M., Raja, E. A., Bhattacharya, S., McNeill, G., Hannaford, P. C., Sarwar, N., Lee, A. J., Bhattacharya, S., & Norman, J. E. (2013) · BMJ · doi:10.1136/bmj.f4539 · Cited by 571 · see citing works
Mookerjee, S. A., Gerencser, A. A., Nicholls, D. G., & Brand, M. D. (2017) · Journal of Biological Chemistry · doi:10.1074/jbc.m116.774471 · Cited by 550 · see citing works
Metabolic Mechanisms in Heart Failure
Ashrafian, H., Frenneaux, M. P., & Opie, L. H. (2007) · Circulation · doi:10.1161/circulationaha.107.702795 · Cited by 517 · see citing works
Mitochondrial biogenesis and dynamics in the developing and diseased heart
Dorn, G. W., Vega, R. B., & Kelly, D. P. (2015) · Genes & Development · doi:10.1101/gad.269894.115 · Cited by 470 · see citing works
Mitochondrial Function, Biology, and Role in Disease
Murphy, E., Ardehali, H., Balaban, R. S., DiLisa, F., Dorn, G. W., Kitsis, R. N., Otsu, K., Ping, P., Rizzuto, R., Sack, M. N., et al. (2016) · Circulation Research · doi:10.1161/res.0000000000000104 · Cited by 459 · see citing works
Clausen, T. D., Mathiesen, E. R., Hansen, T., Pedersen, O., Jensen, D. M., Lauenborg, J., Schmidt, L., & Damm, P. (2009) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2009-0305 · Cited by 453 · see citing works
Ryckman, K. K., Spracklen, C., Smith, C. Z. A., Robinson, J. G., & Saftlas, A. (2015) · BJOG An International Journal of Obstetrics & Gynaecology · doi:10.1111/1471-0528.13261 · Cited by 400 · see citing works
Mitochondria: A central target for sex differences in pathologies
Ventura-Clapier, R., Moulin, M., Piquereau, J., Lemaire, C., Mericskay, M., Veksler, V., & Garnier, A. (2017) · Clinical Science · doi:10.1042/cs20160485 · Cited by 371 · see citing works
Quantitative electron microscopic description of heart muscle cells
Page, E., & McCallister, L. P. (1973) · The American Journal of Cardiology · doi:10.1016/0002-9149(73)91030-8 · Cited by 370 · see citing works
Sex differences in risk factors for myocardial infarction: cohort study of UK Biobank participants
Millett, E. R. C., Peters, S. A. E., & Woodward, M. (2018) · BMJ · doi:10.1136/bmj.k4247 · Cited by 365 · see citing works
Salabei, J. K., Gibb, A., & Hill, B. G. (2014) · Nature Protocols · doi:10.1038/nprot.2014.018 · Cited by 326 · see citing works
Kang, P. M., Haunstetter, A., Aoki, H., Usheva, A., & Izumo, S. (2000) · Circulation Research · doi:10.1161/01.res.87.2.118 · Cited by 323 · see citing works
Developmental Programming in Response to Maternal Overnutrition
Alfaradhi, M. Z., & Ozanne, S. E. (2011) · Frontiers in Genetics · doi:10.3389/fgene.2011.00027 · Cited by 311 · see citing works
Yu, Y., Arah, O. A., Liew, Z., Cnattingius, S., Olsen, J., Sørensen, H. T., Qin, G., & Li, J. (2019) · BMJ · doi:10.1136/bmj.l6398 · Cited by 305 · see citing works
Developmental origins of health and disease (DOHaD)
Silveira, P. P., Portella, A. K., Goldani, M. Z., & Barbieri, M. A. (2007) · Jornal de Pediatria · doi:10.2223/jped.1728 · Cited by 267 · see citing works
Autophagy in Cardiovascular Aging
Abdellatif, M., Sedej, S., Carmona-Gutierrez, D., Madeo, F., & Kroemer, G. (2018) · Circulation Research · doi:10.1161/circresaha.118.312208 · Cited by 239 · see citing works
Evolving and Expanding the Roles of Mitophagy as a Homeostatic and Pathogenic Process
Gustafsson, Å. B., & Dorn, G. W. (2018) · Physiological Reviews · doi:10.1152/physrev.00005.2018 · Cited by 229 · see citing works
Agarwal, P., Morriseau, T. S., Kereliuk, S. M., Doucette, C. A., Wicklow, B. A., & Dolinsky, V. W. (2018) · Critical Reviews in Clinical Laboratory Sciences · doi:10.1080/10408363.2017.1422109 · Cited by 202 · see citing works
Mitochondrial Dynamics in Stem Cells and Differentiation
Seo, B. J., Yoon, S. H., & Tae, J. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19123893 · Cited by 201 · see citing works
Mitophagy Is Required for Acute Cardioprotection by Simvastatin
Andres, A. M., Hernandez, G., Lee, P., Huang, C., Ratliff, E. P., Sin, J., Thornton, C. A., Damasco, M. V., & Gottlieb, R. A. (2013) · Antioxidants and Redox Signaling · doi:10.1089/ars.2013.5416 · Cited by 189 · see citing works
Evolving Concepts of Mitochondrial Dynamics
Dorn, G. W. (2018) · Annual Review of Physiology · doi:10.1146/annurev-physiol-020518-114358 · Cited by 187 · see citing works
Offspring of diabetic pregnancy: Long-term outcomes
Siméoni, U., & Barker, D. J. P. (2009) · Seminars in Fetal and Neonatal Medicine · doi:10.1016/j.siny.2009.01.002 · Cited by 186 · see citing works
Metabolic and genetic regulation of cardiac energy substrate preference
Kodde, I. F., van der Stok, J., Smolenski, R. T., & de Jong, J. W. (2006) · Comparative Biochemistry and Physiology Part A Molecular & Integrative Physiology · doi:10.1016/j.cbpa.2006.09.014 · Cited by 180 · see citing works
Głowińska‐Olszewska, B., Urban, M., Peczyńska, J., & Florys, B. (2005) · Metabolism · doi:10.1016/j.metabol.2005.03.004 · Cited by 175 · see citing works
Hollander, J. M., Thapa, D., & Shepherd, D. L. (2014) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00747.2013 · Cited by 171 · see citing works
VDAC1 at the crossroads of cell metabolism, apoptosis and cell stress
Shoshan-Barmatz, V., N. Maldonado, E., & Krelin, Y. (2017) · Cell Stress · doi:10.15698/cst2017.10.104 · Cited by 170 · see citing works
Determining Maximum Glycolytic Capacity Using Extracellular Flux Measurements
Mookerjee, S. A., Nicholls, D. G., & Brand, M. D. (2016) · PLoS ONE · doi:10.1371/journal.pone.0152016 · Cited by 167 · see citing works
Tomasello, F., Messina, A., Lartigue, L., Schembri, L., Medina, C., Reina, S., Thoraval, D., Crouzet, M., Ichas, F., De Pinto, V., et al. (2009) · Cell Research · doi:10.1038/cr.2009.98 · Cited by 161 · see citing works
Roles of mitochondrial dynamics modulators in cardiac ischaemia/reperfusion injury
Maneechote, C., Palee, S., Chattipakorn, S. C., & Chattipakorn, N. (2017) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.13330 · Cited by 151 · see citing works
Superior Intrinsic Mitochondrial Respiration in Women Than in Men
Cardinale, D. A., Larsen, F. J., Schiffer, T. A., Morales‐Álamo, D., Ekblom, B. T., Calbet, J. A. L., Holmberg, H., & Boushel, R. (2018) · Frontiers in Physiology · doi:10.3389/fphys.2018.01133 · Cited by 136 · see citing works
Intracellular pH Modulates Autophagy and Mitophagy
Berezhnov, A. V., Soutar, M. P. M., Fedotova, E. I., Frolova, M. S., Plun‐Favreau, H., Zinchenko, V. P., & Abramov, A. Y. (2016) · Journal of Biological Chemistry · doi:10.1074/jbc.m115.691774 · Cited by 134 · see citing works
Mitochondrial fission‐fusion as an emerging key regulator of cell proliferation and differentiation
Mitra, K. (2013) · BioEssays · doi:10.1002/bies.201300011 · Cited by 132 · see citing works
Chapter 16 Methods for Distinguishing Apoptotic from Necrotic Cells and Measuring Their Clearance
Krysko, D. V., Berghe, T. V., Parthoens, E., D'Herde, K. G. M. A., & Vandenabeele, P. (2008) · Methods in enzymology on CD-ROM/Methods in enzymology · doi:10.1016/s0076-6879(08)01416-x · Cited by 132 · see citing works
ATM mediates spermidine-induced mitophagy via PINK1 and Parkin regulation in human fibroblasts
Qi, Y., Qiu, Q., Gu, X., Tian, Y., & Zhang, Y. (2016) · Scientific Reports · doi:10.1038/srep24700 · Cited by 122 · see citing works
Cardiac Metabolism in Myocardial Ischemia
Rosano, G. M. C., Fini, M., Caminiti, G., & Bárbaro, G. (2008) · Current Pharmaceutical Design · doi:10.2174/138161208786071317 · Cited by 120 · see citing works
Maternal obesity, lipotoxicity and cardiovascular diseases in offspring
Dong, M., Zheng, Q., Ford, S. P., Nathanielsz, P. W., & Ren, J. T. (2012) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2012.08.023 · Cited by 118 · see citing works
Cyclophilin D, Somehow a Master Regulator of Mitochondrial Function
Porter, G. A., & Beutner, G. (2018) · Biomolecules · doi:10.3390/biom8040176 · Cited by 114 · see citing works
Shelley, P., Martin‐Gronert, M. S., Rowlerson, A. M., Poston, L., Heales, S., Hargreaves, I. P., McConnell, J. M. L., Ozanne, S. E., & Fernandez‐Twinn, D. S. (2009) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00146.2009 · Cited by 107 · see citing works
Mitochondrial-Shaping Proteins in Cardiac Health and Disease – the Long and the Short of It!
Ong, S., Kalkhoran, S. B., Hernández‐Reséndiz, S., Samangouei, P., Ong, S., & Hausenloy, D. J. (2017) · Cardiovascular Drugs and Therapy · doi:10.1007/s10557-016-6710-1 · Cited by 99 · see citing works
Mdaki, K. S., Larsen, T. D., Wachal, A. L., Schimelpfenig, M. D., Weaver, L. J., Dooyema, S. D. R., Louwagie, E. J., & Baack, M. L. (2016) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00795.2015 · Cited by 94 · see citing works
Self-citationSignificant role of estrogen in maintaining cardiac mitochondrial functions
Rattanasopa, C., Phungphong, S., Wattanapermpool, J., & Bupha‐Intr, T. (2014) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/j.jsbmb.2014.11.009 · Cited by 88 · see citing works
Sexual Dimorphism in the Expression of Mitochondria-Related Genes in Rat Heart at Different Ages
Vijay, V., Han, T., Moland, C. L., Kwekel, J. C., Fuscoe, J. C., & Desai, V. G. (2015) · PLoS ONE · doi:10.1371/journal.pone.0117047 · Cited by 81 · see citing works
Necrotic pyknosis is a morphologically and biochemically distinct event from apoptotic pyknosis
Hou, L., Liu, K., Li, Y., Ma, S., Ji, X., & Liu, L. (2016) · Journal of Cell Science · doi:10.1242/jcs.184374 · Cited by 80 · see citing works
Intracellular pH Modulates Autophagy and Mitophagy
Berezhnov, A., Soutar, M. P. M., Fedotova, E., Frolova, M., Plun‐Favreau, H., Zinchenko, V., & Abramov, A. Y. (2016) · UCL Discovery (University College London) · Cited by 80 · see citing works
Developmental programming of mitochondrial biology: a conceptual framework and review
Gyllenhammer, L. E., Entringer, S., Buß, C., & Wadhwa, P. D. (2020) · Proceedings of the Royal Society B Biological Sciences · doi:10.1098/rspb.2019.2713 · Cited by 72 · see citing works
Ferey, J. L. A., Boudoures, A. L., Reid, M., Drury, A. M., Scheaffer, S. M., Modi, Z. N., Kovács, A. D., Pietka, T., DeBosch, B. J., Thompson, M. D., et al. (2019) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00013.2019 · Cited by 67 · see citing works
Maternal malnutrition programs pancreatic islet mitochondrial dysfunction in the adult offspring
Theys, N., Ahn, M., Bouckenooghe, T., Reusens, B., & Remacle, C. (2010) · The Journal of Nutritional Biochemistry · doi:10.1016/j.jnutbio.2010.08.015 · Cited by 65 · see citing works
Infants of diabetic mothers: echocardiographic measurements and cord blood IGF-I and IGFBP-1
El-Ganzoury, M. M., El-Masry, S. A., El-Farrash, R. A., Anwar, M., & Ellatife, R. Z. A. (2011) · Pediatric Diabetes · doi:10.1111/j.1399-5448.2011.00811.x · Cited by 60 · see citing works
Friedman, J. E. (2015) · Diabetes Care · doi:10.2337/dc15-0628 · Cited by 59 · see citing works
Mitophagy as a Protective Mechanism against Myocardial Stress
Nah, J., Miyamoto, S., & Sadoshima, J. (2017) · Comprehensive physiology · doi:10.1002/cphy.c170005 · Cited by 59 · see citing works
Metabolic and Mechanical Cues Regulating Pluripotent Stem Cell Fate
Perestrelo, T., Correia, M., Ramalho‐Santos, J., & Wirtz, D. (2018) · Trends in Cell Biology · doi:10.1016/j.tcb.2018.09.005 · Cited by 57 · see citing works
Barbour, L. A. (2019) · Diabetes Care · doi:10.2337/dci18-0048 · Cited by 57 · see citing works
Larsen, T. D., Sabey, K. H., Knutson, A. J., Gandy, T. C. T., Louwagie, E. J., Lauterboeck, L., Mdaki, K. S., & Baack, M. L. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20123090 · Cited by 57 · see citing works
Self-citationEffects of maternal diabetes and fetal sex on human placenta mitochondrial biogenesis
Jiang, S., Teague, A. M., Tryggestad, J. B., Aston, C. E., Lyons, T. J., & Chernausek, S. D. (2017) · Placenta · doi:10.1016/j.placenta.2017.06.001 · Cited by 52 · see citing works
Long-term cardiovascular risk in relation to birth weight and exposure to maternal diabetes mellitus
Stuart, A., Amer‐Wåhlin, I., Persson, J., & Källén, K. (2013) · International Journal of Cardiology · doi:10.1016/j.ijcard.2013.03.032 · Cited by 51 · see citing works
Female Heart Health: Is GPER the Missing Link?
Groban, L., Tran, Q., Ferrario, C. M., Sun, X., Cheng, C. P., Kitzman, D. W., Wang, H., & Lindsey, S. H. (2020) · Frontiers in Endocrinology · doi:10.3389/fendo.2019.00919 · Cited by 47 · see citing works
Assessment of Fatty Acid Beta Oxidation in Cells and Isolated Mitochondria
Rogers, G. W., Nadanaciva, S., Swiss, R. L., Divakaruni, A. S., & Will, Y. (2014) · Current Protocols in Toxicology · doi:10.1002/0471140856.tx2503s60 · Cited by 46 · see citing works
Ren, Y., Zhou, Q., Yan, Y., Chen, C., Gui, Y., & Li, X. (2011) · Prenatal Diagnosis · doi:10.1002/pd.2717 · Cited by 46 · see citing works
Garg, S., Sharma, P., Sharma, D., Behera, V., Durairaj, M., & Dhall, A. (2014) · Journal of Ultrasound in Medicine · doi:10.7863/ultra.33.8.1365 · Cited by 46 · see citing works
Gao, L., Zhao, Y., Liang, Y., Lin, X., Tan, Y., Wu, D., Li, X., Ye, B., Kong, F., Sheng, J., et al. (2016) · Journal of Pineal Research · doi:10.1111/jpi.12351 · Cited by 42 · see citing works
Ueno, M., Suzuki, J., Hirose, M., Sato, S., Imagawa, M., Zenimaru, Y., Takahashi, S., Ikuyama, S., Koizumi, T., Konoshita, T., et al. (2017) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00098.2017 · Cited by 42 · see citing works
Upadhyaya, B., Larsen, T., Barwari, S., Louwagie, E., Baack, M., & Dey, M. (2017) · Nutrients · doi:10.3390/nu9040407 · Cited by 40 · see citing works
Self-citationConsequences of a Maternal High-Fat Diet and Late Gestation Diabetes on the Developing Rat Lung
Baack, M. L., Forred, B. J., Larsen, T. D., Jensen, D. N., Wachal, A. L., Khan, M. A., & Vitiello, P. F. (2016) · PLoS ONE · doi:10.1371/journal.pone.0160818 · Cited by 40 · see citing works
Self-citationPlacental lipid processing in response to a maternal high-fat diet and diabetes in rats
Louwagie, E. J., Larsen, T. D., Wachal, A. L., & Baack, M. L. (2017) · Pediatric Research · doi:10.1038/pr.2017.288 · Cited by 37 · see citing works
Self-citationAge Related Bioenergetics Profiles in Isolated Rat Cardiomyocytes Using Extracellular Flux Analyses
Mdaki, K. S., Larsen, T. D., Weaver, L. J., & Baack, M. L. (2016) · PLoS ONE · doi:10.1371/journal.pone.0149002 · Cited by 33 · see citing works
Self-citationZablah, J. E., Gruber, D., Stoffels, G. J., Cabezas, E. G., & Hayes, D. A. (2017) · Pediatric Cardiology · doi:10.1007/s00246-017-1584-y · Cited by 31 · see citing works
Yuan, Y., & Pan, S.-S. (2018) · Journal of Cardiovascular Pharmacology · doi:10.1097/fjc.0000000000000572 · Cited by 30 · see citing works
Mortensen, O. H., Larsen, L. H., Ørstrup, L. K. H., Hansen, L. H. L., Grunnet, N., & Quistorff, B. (2014) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1038/jcbfm.2014.72 · Cited by 27 · see citing works
Cardiac Glucolipotoxicity and Cardiovascular Outcomes
Cerf, M. E. (2018) · Medicina · doi:10.3390/medicina54050070 · Cited by 25 · see citing works
Response characteristics of the mitochondrial DNA genome in developmental health and disease
Knudsen, T. B., & Green, M. L. (2004) · Birth Defects Research Part C Embryo Today Reviews · doi:10.1002/bdrc.20028 · Cited by 17 · see citing works
Prevalence of Pre-pregnancy Obesity, 2011-2014.
Gregor, L., Remington, P., Lindberg, S. M., & Ehrenthal, D. B. (2016) · PubMed · Cited by 16 · see citing works
Cardiac Energy Metabolism in Health and Disease
Lopaschuk, G. D., & Dhalla, N. S. (2014) · Springer eBooks · doi:10.1007/978-1-4939-1227-8 · Cited by 14 · see citing works
Is the child at risk? Cardiovascular remodelling in children born to diabetic mothers
Hoodbhoy, Z. A., Mohammed, N., Aslam, N., Fatima, U., Ashiqali, S., Rizvi, A., Pascua, C. J., Chowdhury, D., & Hasan, B. S. (2019) · Cardiology in the Young · doi:10.1017/s1047951119000040 · Cited by 13 · see citing works
Zhu, M., Lu, J., Pan, G., Song, P., Zhao, F., Qi, H.-T., Hai-ya, Y., Xu, J. C., Wan, G., & Li, P. (2017) · Oncotarget · doi:10.18632/oncotarget.18041 · Cited by 12 · see citing works
[The role of diabetes mellitus as a risk factor of acute myocardial infarction].
Peng, X.-R., Zhao, Y., Zou, D., & Gu, P. (2011) · PubMed · Cited by 7 · see citing works
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Louwagie, E. J., Larsen, T. D., Wachal, A. L., Gandy, T. C. T., & Baack, M. L. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22052382 · Cited by 43 · see citing works
Self-citationKereliuk, S. M., & Dolinsky, V. W. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23084467 · Cited by 34 · see citing works
“Male offspring exhibited reduced diastolic function without systolic impairments, while female offspring exhibited systolic dysfunction, but not diastolic dysfunction, compared to controls [111].”
BackgroundResultInfluentialThe sex-dependent response to psychosocial stress and ischaemic heart disease
Helman, T. J., Headrick, J. P., Stapelberg, N. J. C., & Braidy, N. (2023) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2023.1072042 · Cited by 34 · see citing works
Tocantins, C., Diniz, M. S., Grilo, L. F., & Pereira, S. P. (2022) · WIREs Mechanisms of Disease · doi:10.1002/wsbm.1555 · Cited by 28 · see citing works
Mitochondrial Quality Control Mechanisms during Diabetic Cardiomyopathy
Ketenci, M., Zablocki, D., & Sadoshima, J. (2022) · JMA Journal · doi:10.31662/jmaj.2022-0155 · Cited by 21 · see citing works
Cao, Y., Dong, Z., Yang, D., Ma, X., & Wang, X. (2021) · Chemistry and Physics of Lipids · doi:10.1016/j.chemphyslip.2021.105138 · Cited by 19 · see citing works
Long-term outcomes and potential mechanisms of offspring exposed to intrauterine hyperglycemia
Yan, Y., Feng, C., Yu, D., Tian, S., Zhou, Y. X., Huang, Y.-T., Cai, Y., Chen, J., Zhu, M., & Jin, M. (2023) · Frontiers in Nutrition · doi:10.3389/fnut.2023.1067282 · Cited by 21 · see citing works
Calderón‐Garcidueñas, L., González-Maciel, A., Reynoso-Robles, R., Rodríguez‐López, J. L., Silva-Pereyra, H. G., Labrada-Delgado, G. J., Pérez-Guillé, B., Soriano‐Rosales, R. E., Luna, M. A. J.-B., Brito-Aguilar, R., et al. (2021) · Environmental Science & Technology · doi:10.1021/acs.est.1c01733 · Cited by 17 · see citing works
Research Progress of Maternal Metabolism on Cardiac Development and Function in Offspring
Ren, Z., Luo, S., Cui, J., Tang, Y., Huang, H., & Ding, G. (2023) · Nutrients · doi:10.3390/nu15153388 · Cited by 16 · see citing works
Davies, K., Camm, E. J., Smith, D. J., Miles, J., Forhead, A. J., Murray, A. J., & Fowden, A. L. (2022) · Journal of Developmental Origins of Health and Disease · doi:10.1017/s204017442200040x · Cited by 7 · see citing works
Guidelines for in vivo models of developmental programming of cardiovascular disease risk
Warrington, J. P., Collins, H. E., Davidge, S. T., do Carmo, J. M., Goulopoulou, S., Intapad, S., Loria, A. S., Sones, J. L., Wold, L. E., Zinkhan, E. K., et al. (2024) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00060.2024 · Cited by 4 · see citing works
Siemers, K. M., Joss‐Moore, L. A., & Baack, M. L. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252111534 · Cited by 4 · see citing works
Self-citationKlein, A. K., Derenge, B. P., Mukherjee, M., Reddy, S. P., Larsen, T. D., Ayyappan, P., Gandy, T. C. T., Siemers, K. M., Kareta, M. S., & Baack, M. L. (2025) · Biomedicines · doi:10.3390/biomedicines13082019 · Cited by 3 · see citing works
Self-citationZhang, J., Wang, J., Xu, D., Gui, Y., Bai, F., Huo, Y., Cao, L., & Gui, Y. (2024) · Nutrients · doi:10.3390/nu16152520 · Cited by 2 · see citing works
Ayyappan, P., Larsen, T. D., Gandy, T. C. T., Louwagie, E. J., & Baack, M. L. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24043684 · Cited by 2 · see citing works
Self-citationMitochondria as a Therapeutic Target in Metabolic Disorders
Cai, Y., Gan, F., Chen, Y., He, Q., Chen, W., Peng, Z., & Gong, L. (2025) · Mini-Reviews in Medicinal Chemistry · doi:10.2174/0113895575403490250917111723 · Cited by 1 · see citing works
Clavier, A., Graf, S., Helmer, A., Lagger, D., Egle, M., Segiser, A., Siepe, M., Arnold, M., & Longnus, S. (2025) · Scientific Reports · doi:10.1038/s41598-025-28644-9 · Cited by 1 · see citing works
Diabetes and mitochondrial transplantation
Louwagie, E. J., & Baack, M. L. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-18858-9.00022-6
Self-citationAyyappan, P., Gandy, T. C. T., Sturdevant, D. A., Larsen, T. D., Mukuntharaj, P., Paulson, A., Christensen, T. A., Salisbury, J. L., & Baack, M. L. (2025) · Cells · doi:10.3390/cells14211698
Self-citationMitochondrial Dysfunction: A Critical Link Between Maternal Diet and Offspring Metabolic Health
Shao, C., Lin, H., Yu, J., Chen, H., Ren, Y., Ren, J., Zeng, Y., Wu, Y., Zhang, Q., & Xiao, X. (2026) · Biomolecules · doi:10.3390/biom16081106
- Authors
- Louwagie, E. J., Larsen, T. D., Wachal, A. L., Gandy, T. C. T., Eclov, J. A., Rideout, T. C., Kern, K. A., Cain, J. T., Anderson, R. H., Mdaki, K. S., & Baack, M. L.
- Affiliations
- University of South Dakota (US)
- Sanford Research (US)
- University at Buffalo, State University of New York (US)
- Sanford Health (US)
- Corresponding author
- Louwagie, Eli J.
- Baack, Michelle L.
- ORCID
- Venue
- iScience
- Publisher
- Elsevier BV
- Published
- 2020-11
- Volume
- 23
- Issue
- 11
- Pages
- 101746
- ISSN
- 2589-0042 (ISSN-L)
- PMC
- PMC7666357
- OpenAlex
- W3097288581
- Cited by
- 20
- References
- 87
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 4 · 2023: 4 · 2022: 4 · 2021: 3
- FWCI
- 2.64
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- iScience (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- National Institute of General Medical Sciences
- National Science Foundation
- National Institute of Child Health and Human Development
- National Center for Complementary and Integrative Health
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Keywords
- diabetes in pregnancy, cardiomyopathy, mitochondrial dysfunction, mitophagy, oxidative phosphorylation, mitochondrial turnover, mitochondrial membrane potential, metabolic stress, mitochondrial cell death, sex differences, cross-fostering
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