Incidences of genomic alterations are equally frequent in aging, metabolic disorders, and cancer. Diverse intrinsic and extrinsic/environmental factors often cause genotoxicity and produce etiologically unique and intersecting genomic signatures, as reflected in their overlapping heritage in aging, metabolic disorders, and cancer. Given the fact that genomic integrity and its proofreading abilities gradually decline with organism lifespan, the burden of these alterations elevates significantly with the progressive aging that may also potentiate metabolic disorders. While recent evidence, on contrary, hinted at the role of metabolic perturbations in accelerated aging. In both ways, interactions among diverse factors/components in aging, metabolism, and redox biology (including mitochondria fitness, Ca2+ signaling, bioenergetics) are evident and can be annotated to their genomic origin. Irreversible genomic aberrations are often seen to potentiate cancer progression, which is notoriously more prevalent with aging, and thus, these states are at the crossroads at multiple points. For instance, the occurrence of aberrant mitochondrial mutations in aging and cancer, while an altered metabolic reprogramming takes place in a cancer cell. Given the stochastic nature of genomic perturbations in cancer, its origin is referred to as heterogeneous and multifactorial and thus warranted a need to attain a greater diagnostic/therapeutic resolution. In this line, revised interventional strategies including precision-based therapeutics are now being considered promising.
In this series, we aim to connect multiple dots in the evolving knowledge of genomic alterations in aging, metabolic disorders, and cancer by shedding light on their emerging overlaps and clinical importance.
We welcome researchers working in these domains to contribute with the Original Research, Methods, Review, and Mini-Review, Hypothesis/Theory, Data/Research Reports, Perspectives/Opinions, and Commentaries. Besides the exciting research in the specialized aging, metabolic disorders, and cancer domains, we specifically welcome submissions highlighting their emerging overlaps and clinical importance. We target, yet not limited, to cover the following non-exhaustive list of sub-themes:
1. Genomic alterations and perturbed signaling pathways in aging and their functional significance.
2. Present outlook and crossroad of altered metabolic and oncogenic pathways and their function.
3. Mitochondrial dysfunctions in metabolic disorders, cardiovascular disorders, aging, and cancer.
4. REDOX and intracellular ionic homeostasis in organ-specific metabolic dysfunctions and outcomes in whole-body metabolic homeostasis.
5. Role of Metabolic stress in supporting cancer cell survival and proliferation.
6. Targeting cancer metabolism for cancer therapy and personalized therapeutic target(s).
7. Genetic basis of metabolic and cardiovascular disease and involved molecular signaling(s).
8. Cardiometabolic disease and its consequences on associated organ system(s).
Incidences of genomic alterations are equally frequent in aging, metabolic disorders, and cancer. Diverse intrinsic and extrinsic/environmental factors often cause genotoxicity and produce etiologically unique and intersecting genomic signatures, as reflected in their overlapping heritage in aging, metabolic disorders, and cancer. Given the fact that genomic integrity and its proofreading abilities gradually decline with organism lifespan, the burden of these alterations elevates significantly with the progressive aging that may also potentiate metabolic disorders. While recent evidence, on contrary, hinted at the role of metabolic perturbations in accelerated aging. In both ways, interactions among diverse factors/components in aging, metabolism, and redox biology (including mitochondria fitness, Ca2+ signaling, bioenergetics) are evident and can be annotated to their genomic origin. Irreversible genomic aberrations are often seen to potentiate cancer progression, which is notoriously more prevalent with aging, and thus, these states are at the crossroads at multiple points. For instance, the occurrence of aberrant mitochondrial mutations in aging and cancer, while an altered metabolic reprogramming takes place in a cancer cell. Given the stochastic nature of genomic perturbations in cancer, its origin is referred to as heterogeneous and multifactorial and thus warranted a need to attain a greater diagnostic/therapeutic resolution. In this line, revised interventional strategies including precision-based therapeutics are now being considered promising.
In this series, we aim to connect multiple dots in the evolving knowledge of genomic alterations in aging, metabolic disorders, and cancer by shedding light on their emerging overlaps and clinical importance.
We welcome researchers working in these domains to contribute with the Original Research, Methods, Review, and Mini-Review, Hypothesis/Theory, Data/Research Reports, Perspectives/Opinions, and Commentaries. Besides the exciting research in the specialized aging, metabolic disorders, and cancer domains, we specifically welcome submissions highlighting their emerging overlaps and clinical importance. We target, yet not limited, to cover the following non-exhaustive list of sub-themes:
1. Genomic alterations and perturbed signaling pathways in aging and their functional significance.
2. Present outlook and crossroad of altered metabolic and oncogenic pathways and their function.
3. Mitochondrial dysfunctions in metabolic disorders, cardiovascular disorders, aging, and cancer.
4. REDOX and intracellular ionic homeostasis in organ-specific metabolic dysfunctions and outcomes in whole-body metabolic homeostasis.
5. Role of Metabolic stress in supporting cancer cell survival and proliferation.
6. Targeting cancer metabolism for cancer therapy and personalized therapeutic target(s).
7. Genetic basis of metabolic and cardiovascular disease and involved molecular signaling(s).
8. Cardiometabolic disease and its consequences on associated organ system(s).