Understanding lamin proteins and their roles in aging and cardiovascular diseases

Jiang, Yizhi; Ji, Julie Y.

doi:10.1016/j.lfs.2018.09.026

Cited by 15 publications

(7 citation statements)

References 211 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Since Klotho has the kidney defence ability (Morales et al 1996, for example) it should promote chronic renal illness through improper tissue healing and poor damage protection. The elevated amount of casapase 14, a protein that is implicated in apoptosis and prelamin A/C in CF exosomes, as accumulation of lamina proteins in different neurodegenerative illnesses (Jiang & Ji 2018), also suggests this "accelerated ageing" problem (Le Dour et al, 2017). Our findings also demonstrated that proteins and gene sets in urine exosomal matrisomes were consistently downregulated.…”

Section: Tissue Repair Dysregulation and A Potential Pro-aging Cf Dis...supporting

confidence: 55%

Biochemical Aspects of Cystic Fibrosis and Kidney Disease: A Brief Discussion

Sabih

Mahmood

Jahangeer

et al. 2021

FCS

View full text Add to dashboard Cite

Cystic fibrosis is a recessive autosomal disease. A nosographic entity that considered lethal in childhood. In organs such as the hypothalamus, kidney, and bone, the protein is directly affected, where its malfunction is likely to imply linear delays in growth, delayed pubertal onset, modulation of bone density, and susceptibility to renal calculus, which may be present in CF and have been in use for years, Nevertheless, the most researched and recognized cause of renal wound is iatrogenic in CF patients due to the consumption by pulmonary exacerbation of large doses of aminoglycosides (3-5 mg/kg/dose). The rise in the incidence of CF nephrocalcinosis does not seem to be connected to an inherent renal issue. Among fact, chronic kidney disease (CKD) prevalence in CF patients looks to be at least twice as high with a double rise every 10 years impacting over 20% of individuals older than 55 years. There has been no substantial change in proteome content in the treatment of CFTR modulators. These data indicate that a re-regulating proteasome activities adapts CF cells to the CFTR deficiency and impairs autophagy and endosomal aiming.

show abstract

Section: Tissue Repair Dysregulation and A Potential Pro-aging Cf Dis...supporting

confidence: 55%

Biochemical Aspects of Cystic Fibrosis and Kidney Disease: A Brief Discussion

Sabih

Mahmood

Jahangeer

et al. 2021

FCS

View full text Add to dashboard Cite

show abstract

“…As Klotho is involved in the kidney's ability to defend against renal insults [5], this defect should favor chronic kidney disease by abnormal tissue repair and defective protection against damage. This "accelerated aging" defect is also suggested by the increased level of caspase 14, a protein involved in apoptosis and of prelamin A/C in CF exosome, as accumulation of lamin proteins, are involved in various neurodegenerative diseases [28,29].…”

Section: Dysregulated Tissue Repair and Potential Pro-aging Cf Diseasmentioning

confidence: 95%

Urinary Exosomes of Patients with Cystic Fibrosis Unravel CFTR-Related Renal Disease

Gauthier

Pranke

Jung

et al. 2020

IJMS

View full text Add to dashboard Cite

Background: The prevalence of chronic kidney disease is increased in patients with cystic fibrosis (CF). The study of urinary exosomal proteins might provide insight into the pathophysiology of CF kidney disease. Methods: Urine samples were collected from 19 CF patients (among those 7 were treated by cystic fibrosis transmembrane conductance regulator (CFTR) modulators), and 8 healthy subjects. Urine exosomal protein content was determined by high resolution mass spectrometry. Results: A heatmap of the differentially expressed proteins in urinary exosomes showed a clear separation between control and CF patients. Seventeen proteins were upregulated in CF patients (including epidermal growth factor receptor (EGFR); proteasome subunit beta type-6, transglutaminases, caspase 14) and 118 were downregulated (including glutathione S-transferases, superoxide dismutase, klotho, endosomal sorting complex required for transport, and matrisome proteins). Gene set enrichment analysis revealed 20 gene sets upregulated and 74 downregulated. Treatment with CFTR modulators yielded no significant modification of the proteomic content. These results highlight that CF kidney cells adapt to the CFTR defect by upregulating proteasome activity and that autophagy and endosomal targeting are impaired. Increased expression of EGFR and decreased expression of klotho and matrisome might play a central role in this CF kidney signature by inducing oxidation, inflammation, accelerated senescence, and abnormal tissue repair. Conclusions: Our study unravels novel insights into consequences of CFTR dysfunction in the urinary tract, some of which may have clinical and therapeutic implications.

show abstract

“…The complexity of atherosclerosis involves many factors in addition to prelamin A in VSMC, foam cells, and endothelial cells as described in many articles [45,53,54]. The review of the role of lamins in atherosclerosis by Jiang and Ji provides additional useful information [55]. AGING…”

Section: Vascular Smooth Muscle Cellsmentioning

confidence: 99%

Lamin A to Z in normal aging

Primmer

Liao

Kummert

et al. 2022

Aging

View full text Add to dashboard Cite

Almost since the discovery that mutations in the LMNA gene, encoding the nuclear structure components lamin A and C, lead to Hutchinson-Gilford progeria syndrome, people have speculated that lamins may have a role in normal aging. The most common HPGS mutation creates a splice variant of lamin A, progerin, which promotes accelerated aging pathology. While some evidence exists that progerin accumulates with normal aging, an increasing body of work indicates that prelamin A, a precursor of lamin A prior to C-terminal proteolytic processing, accumulates with age and may be a driver of normal aging. Prelamin A shares properties with progerin and is also linked to a rare progeroid disease, restrictive dermopathy. Here, we describe mechanisms underlying changes in prelamin A with aging and lay out the case that this unprocessed protein impacts normative aging. This is important since intervention strategies can be developed to modify this pathway as a means to extend healthspan and lifespan.

show abstract

Understanding lamin proteins and their roles in aging and cardiovascular diseases

Cited by 15 publications

References 211 publications

Biochemical Aspects of Cystic Fibrosis and Kidney Disease: A Brief Discussion

Biochemical Aspects of Cystic Fibrosis and Kidney Disease: A Brief Discussion

Urinary Exosomes of Patients with Cystic Fibrosis Unravel CFTR-Related Renal Disease

Lamin A to Z in normal aging

Contact Info

Product

Resources

About