Reducing the prevalence of chronic kidney disease (CKD), a hidden epidemic affecting over 850 million people worldwide, is hampered by lack of effective therapies and the increased incidence of the disease risk factors and co-morbidities. Inadequate availability of renal replacement therapies to treat the patients with end stage renal disease around the globe also poses an enormous medical burden. CKD prevalence is significantly higher in the aging population and renal aging and senescence are important contributors to fibrosis progression, although the underlying mechanistic links are not well understood.
In this Research Topic, we solicit Original Research articles as well as state of the art Reviews that address the molecular and pathological basis of renal aging and senescence that contribute to renal injury, failed repair and progressive fibrosis. Manuscripts that focus on novel therapies to target the senescent renal cell population as an anti-fibrotic approach are of interest. Articles that address the following themes are encouraged:
1. Targeting the senescence-associated secretory phenotype (SASP) or epithelial tubular cell growth arrest to limit fibrosis and promote renal repair.
2. New approaches to target pathological oxidative stress/associated pathways such as p53, DNA damage response (DDR), tubular dysfunction and maladaptive repair leading to tubular cell senescence/growth arrest.
3. Inflammation, innate immunity, tubular senescence and aging in renal disease.
4. Established and novel mechanisms and pathways that promote premature renal aging. and disease (e.g., Klotho involvement).
5. New animal models to study renal aging and senescence and definition of new renal or urine biomarkers to detect senescence and disease progression.
6. Metabolic alterations and mitochondrial dysfunction in renal aging, senescence and fibrosis.
7. Cross-talk between established fibrotic factors (e.g., TGF-&Beta, CTGF and PAI-1 and novel regulators (e.g., non-transcribed micro- and other RNAs) and methylation in tubular injury/failed repair and senescence.
8. Genetic determinants of DDR-competence and susceptibility to induction of cellular senescence in kidney disease (e.g. CKD development after chemotherapy and irradiation, post ischemia–reperfusion injury, surgery) .
9. Epigenetic factors (miRs, lncRNAs, methylation (e.g. RASL1), chromatin organization) in premature renal aging and disease.
10. The diversity of the senescent phenotype in premature aging of the kidney: overcoming challenges in targeting senescent cells in the context of renal fibrosis in vivo.
Reducing the prevalence of chronic kidney disease (CKD), a hidden epidemic affecting over 850 million people worldwide, is hampered by lack of effective therapies and the increased incidence of the disease risk factors and co-morbidities. Inadequate availability of renal replacement therapies to treat the patients with end stage renal disease around the globe also poses an enormous medical burden. CKD prevalence is significantly higher in the aging population and renal aging and senescence are important contributors to fibrosis progression, although the underlying mechanistic links are not well understood.
In this Research Topic, we solicit Original Research articles as well as state of the art Reviews that address the molecular and pathological basis of renal aging and senescence that contribute to renal injury, failed repair and progressive fibrosis. Manuscripts that focus on novel therapies to target the senescent renal cell population as an anti-fibrotic approach are of interest. Articles that address the following themes are encouraged:
1. Targeting the senescence-associated secretory phenotype (SASP) or epithelial tubular cell growth arrest to limit fibrosis and promote renal repair.
2. New approaches to target pathological oxidative stress/associated pathways such as p53, DNA damage response (DDR), tubular dysfunction and maladaptive repair leading to tubular cell senescence/growth arrest.
3. Inflammation, innate immunity, tubular senescence and aging in renal disease.
4. Established and novel mechanisms and pathways that promote premature renal aging. and disease (e.g., Klotho involvement).
5. New animal models to study renal aging and senescence and definition of new renal or urine biomarkers to detect senescence and disease progression.
6. Metabolic alterations and mitochondrial dysfunction in renal aging, senescence and fibrosis.
7. Cross-talk between established fibrotic factors (e.g., TGF-&Beta, CTGF and PAI-1 and novel regulators (e.g., non-transcribed micro- and other RNAs) and methylation in tubular injury/failed repair and senescence.
8. Genetic determinants of DDR-competence and susceptibility to induction of cellular senescence in kidney disease (e.g. CKD development after chemotherapy and irradiation, post ischemia–reperfusion injury, surgery) .
9. Epigenetic factors (miRs, lncRNAs, methylation (e.g. RASL1), chromatin organization) in premature renal aging and disease.
10. The diversity of the senescent phenotype in premature aging of the kidney: overcoming challenges in targeting senescent cells in the context of renal fibrosis in vivo.
