GLORIA

GEOMAR Library Ocean Research Information Access

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    In: The FASEB Journal, Wiley, Vol. 35, No. S1 ( 2021-05)
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 1468876-1
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    Online Resource
    Online Resource
    OAE Publishing Inc. ; 2022
    In:  The Journal of Cardiovascular Aging ( 2022)
    In: The Journal of Cardiovascular Aging, OAE Publishing Inc., ( 2022)
    Abstract: Aging promotes structural and functional remodeling of the heart, even in the absence of external factors. There is growing clinical and experimental evidence supporting the existence of sex-specific patterns of cardiac aging, and in some cases, these sex differences emerge early in life. Despite efforts to identify sex-specific differences in cardiac aging, understanding how these differences are established and regulated remains limited. In addition to contributing to sex differences in age-related heart disease, sex differences also appear to underlie differential responses to cardiac stress such as adrenergic activation. Identifying the underlying mechanisms of sex-specific differences may facilitate the characterization of underlying heart disease phenotypes, with the ultimate goal of utilizing sex-specific therapeutic approaches for cardiac disease. The purpose of this review is to discuss the mechanisms and implications of sex-specific cardiac aging, how these changes render the heart more susceptible to disease, and how we can target age- and sex-specific differences to advance therapies for both male and female patients.
    Type of Medium: Online Resource
    ISSN: 2768-5993
    Language: Unknown
    Publisher: OAE Publishing Inc.
    Publication Date: 2022
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 3
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 325, No. 2 ( 2023-08-01), p. H278-H292
    Abstract: Right ventricular (RV) function is the strongest predictor of survival in age-related heart failure as well as other clinical contexts in which aging populations suffer significant morbidity and mortality. However, despite the significance of maintaining RV function with age and disease, mechanisms of RV failure remain poorly understood and no RV-directed therapies exist. The antidiabetic drug and AMP-activated protein kinase (AMPK) activator metformin protects against left ventricular dysfunction, suggesting cardioprotective properties may translate to the RV. Here, we aimed to understand the impact of advanced age on pulmonary hypertension (PH)-induced right ventricular dysfunction. We further aimed to test whether metformin is cardioprotective in the RV and whether the protection afforded by metformin requires cardiac AMPK. We used a murine model of PH by exposing adult (4–6 mo) and aged (18 mo) male and female mice to hypobaric hypoxia (HH) for 4 wk. Cardiopulmonary remodeling was exacerbated in aged mice compared with adult mice as evidenced by elevated RV weight and impaired RV systolic function. Metformin attenuated HH-induced RV dysfunction but only in adult male mice. Metformin still protected the adult male RV even in the absence of cardiac AMPK. Together, we suggest that aging exacerbates PH-induced RV remodeling and that metformin may represent a therapeutic option for this disease in a sex- and age-dependent manner, but in an AMPK-independent manner. Ongoing efforts are aimed at elucidating the molecular basis for RV remodeling as well as delineating the mechanisms of cardioprotection provided by metformin in the absence of cardiac AMPK. NEW & NOTEWORTHY Right ventricular (RV) function predicts survival in age-related disease, yet mechanisms of RV failure are unclear. We show that aged mice undergo exacerbated RV remodeling compared with young. We tested the AMPK activator metformin to improve RV function and show that metformin attenuates RV remodeling only in adult male mice via a mechanism that does not require cardiac AMPK. Metformin is therapeutic for RV dysfunction in an age- and sex-specific manner independent of cardiac AMPK.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2023
    detail.hit.zdb_id: 1477308-9
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 4
    In: GeroScience, Springer Science and Business Media LLC
    Type of Medium: Online Resource
    ISSN: 2509-2723
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2886418-9
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 5
    In: Journal of Biological Rhythms, SAGE Publications, Vol. 38, No. 3 ( 2023-06), p. 290-304
    Abstract: Circadian misalignment occurs with age, jet lag, and shift work, leading to maladaptive health outcomes including cardiovascular diseases. Despite the strong link between circadian disruption and heart disease, the cardiac circadian clock is poorly understood, prohibiting identification of therapies to restore the broken clock. Exercise is the most cardioprotective intervention identified to date and has been suggested to reset the circadian clock in other peripheral tissues. Here, we tested the hypothesis that conditional deletion of core circadian gene Bmal1 would disrupt cardiac circadian rhythm and function and that this disruption would be ameliorated by exercise. To test this hypothesis, we generated a transgenic mouse with spatial and temporal deletion of Bmal1 only in adult cardiac myocytes (Bmal1 cardiac knockout [cKO]). Bmal1 cKO mice demonstrated cardiac hypertrophy and fibrosis concomitant with impaired systolic function. This pathological cardiac remodeling was not rescued by wheel running. While the molecular mechanisms responsible for the profound cardiac remodeling are unclear, it does not appear to involve activation of the mammalian target of rapamycin (mTOR) signaling or changes in metabolic gene expression. Interestingly, cardiac deletion of Bmal1 disrupted systemic rhythms as evidenced by changes in the onset and phasing of activity in relationship to the light/dark cycle and by decreased periodogram power as measured by core temperature, suggesting cardiac clocks can regulate systemic circadian output. Together, we suggest a critical role for cardiac Bmal1 in regulating both cardiac and systemic circadian rhythm and function. Ongoing experiments will determine how disruption of the circadian clock causes cardiac remodeling in an effort to identify therapeutics to attenuate the maladaptive outcomes of a broken cardiac circadian clock.
    Type of Medium: Online Resource
    ISSN: 0748-7304 , 1552-4531
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2023
    detail.hit.zdb_id: 2018064-0
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 6
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2021
    In:  Innovation in Aging Vol. 5, No. Supplement_1 ( 2021-12-17), p. 678-678
    In: Innovation in Aging, Oxford University Press (OUP), Vol. 5, No. Supplement_1 ( 2021-12-17), p. 678-678
    Abstract: Cardiovascular disease continues to be a major cause of morbidity and mortality, particularly in aging populations. Exercise is amongst the most cardioprotective interventions identified to date, with early in life exercise such as during the juvenile period potentially imparting even more cardioprotective outcomes due to the plasticity of the developing heart. To test the hypothesis that juvenile exercise would impart later in life cardioprotection, we exercised juvenile male and female mice via voluntary wheel running from 3-5 weeks of age and then exposed them to cardiac stress by isoproterenol (ISO) at 4-6 and 18 months of age in adulthood and older age, respectively. We compared cardiac function and remodeling to sedentary control animals, sedentary animals who received ISO, and adult and aged mice that exercised for two weeks immediately before ISO exposure. Juvenile mice engaged in voluntarily wheel running, with male mice running 1.3 ± 0.8 km and female mice 2.8 ± 1.0 km a day. Echocardiography suggested that these juvenile animals underwent running-induced cardiac remodeling as evidenced by higher ejection fraction and stroke volume compared to sedentary controls. Exercise in the juvenile period attenuated ISO-induced cardiac hypertrophy and remodeling later in life compared to sedentary animals and those that exercised immediately before ISO administration. The mechanisms by which early versus late exercise is protective in adult and aged mice are under investigation. Further ongoing work will identify the adaptations induced by exercise in the juvenile heart that may help improve cardiac aging.
    Type of Medium: Online Resource
    ISSN: 2399-5300
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 2905697-4
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 7
    In: Physiological Reports, Wiley, Vol. 9, No. 13 ( 2021-07)
    Type of Medium: Online Resource
    ISSN: 2051-817X , 2051-817X
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2724325-4
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 8
    Online Resource
    Online Resource
    American Physiological Society ; 2023
    In:  Journal of Applied Physiology Vol. 135, No. 3 ( 2023-09-01), p. 572-583
    In: Journal of Applied Physiology, American Physiological Society, Vol. 135, No. 3 ( 2023-09-01), p. 572-583
    Abstract: Cardiovascular disease is an enormous public health problem, particularly in older populations. Exercise is the most potent cardioprotective intervention identified to date, with exercise in the juvenile period potentially imparting greater protection, given the plasticity of the developing heart. To test the hypothesis that voluntary wheel running early in life would be cardioprotective later in life when risk for disease is high, we provided male and female juvenile (3 wk old) mice access to a running wheel for 2 wk. Mice then returned to a home cage to age to adulthood (4–6 mo) before exposure to isoproterenol (ISO) to induce cardiac stress. Cardiac function and remodeling were compared with sedentary control mice, sedentary mice exposed to ISO, and mice that exercised in adulthood immediately before ISO. Early in life activity protected against ISO-induced stress as evidenced by attenuated cardiac mass, myocyte size, and fibrosis compared with sedentary mice exposed to ISO. ISO-induced changes in cardiac function were ameliorated in male mice that engaged in wheel running, with ejection fraction and fractional shortening reversed to control values. Adrenergic receptor expression was downregulated in juvenile male runners. This suppression persisted in adulthood following ISO, providing a putative mechanism by which exercise in the young male heart provides resilience to cardiac stress later in life. Together, we show that activity early in life induces persistent cardiac changes that attenuate ISO-induced stress in adulthood. Identification of the mechanisms by which early in life exercise is protective will yield valuable insights into how exercise is medicine across the life course. NEW & NOTEWORTHY Voluntary wheel running activity early in life induces persistent changes in the heart that attenuate isoproterenol-induced hypertrophy and fibrosis in adulthood. Though the mechanisms of this protection remain incompletely understood, activity-induced downregulation of adrenergic receptor expression early in life may contribute to later protection against adrenergic stress. Together these data suggest that efforts to maintain an active lifestyle early in life may have long-lasting cardioprotective benefits.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2023
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 9
    In: Genetics, Oxford University Press (OUP), Vol. 212, No. 1 ( 2019-05-01), p. 93-110
    Abstract: A Neurospora meiotic drive element known as Spore killer-2 (Sk-2) achieves biased transmission through sexual reproduction by killing siblings that inherit a competing allele... Sk-2 is a meiotic drive element that was discovered in wild populations of Neurospora fungi over 40 years ago. While early studies quickly determined that Sk-2 transmits itself through sexual reproduction in a biased manner via spore killing, the genetic factors responsible for this phenomenon have remained mostly unknown. Here, we identify and characterize rfk-1, a gene required for Sk-2-based spore killing. The rfk-1 gene contains four exons, three introns, and two stop codons, the first of which undergoes RNA editing to a tryptophan codon during sexual development. Translation of an unedited rfk-1 transcript in vegetative tissue is expected to produce a 102-amino acid protein, whereas translation of an edited rfk-1 transcript in sexual tissue is expected to produce a protein with 130 amino acids. These findings indicate that unedited and edited rfk-1 transcripts exist and that these transcripts could have different roles with respect to the mechanism of meiotic drive by spore killing. Regardless of RNA editing, spore killing only succeeds if rfk-1 transcripts avoid silencing caused by a genome defense process called meiotic silencing by unpaired DNA (MSUD). We show that rfk-1’s MSUD avoidance mechanism is linked to the genomic landscape surrounding the rfk-1 gene, which is located near the Sk-2 border on the right arm of chromosome III. In addition to demonstrating that the location of rfk-1 is critical to spore-killing success, our results add to accumulating evidence that MSUD helps protect Neurospora genomes from complex meiotic drive elements.
    Type of Medium: Online Resource
    ISSN: 1943-2631
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 1477228-0
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 10
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 2021
    In:  GeroScience Vol. 43, No. 4 ( 2021-08), p. 1799-1813
    In: GeroScience, Springer Science and Business Media LLC, Vol. 43, No. 4 ( 2021-08), p. 1799-1813
    Type of Medium: Online Resource
    ISSN: 2509-2715 , 2509-2723
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 2886418-9
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...