Inflammaging, Organism Aging, and Age-Related Chronic Diseases

With the steady growing of the elderly population, aging represents the great challenge for our society and medical care system. Aging is a prominent risk factor for many chronic disease, including cardiovascular disease, metabolic disease, chronic kidney disease, neurological disorders, and cancer.

Many of the mechanisms of organism aging process is common with the pathogenesis of the above mentioned diseases, such as chronic inflammation (inflammaging), cell senescence, cell death, mitochondrial dysfunction, and organ or tissue fibrosis, that lead to organ functional failure. Elucidating mechanisms of aging process and investigating how aging process affects the disease process - and vice versa, will have great impact on extension of healthy lifespan and incidence of the chronical diseases of every organ.

Our current research is to investigate the roles of chronic inflammation, (cellular senescence and secretion of inflammatory cytokines or SASP) and / or hypoxia on aging process. The hypoxia-responsive genes including arginase, HIFs, inflammatory cytokines, etc, in aging process and age-related tissue fibrosis in the heart, kidney, lung, and tumours are investigated using model systems such as cell/tissue culture, genetic modified mouse models, and human biopsies.

The therapeutic effects of targeting these genes either pharmacologically or genetically on organismal aging and age-related diseases are under investigation.

Main lines of research

• Research Interest
  1. Mechanisms of inflammaging and the impact on mitochondrial dysfunction and fibrosis in aging heart and in ischemia/reperfusion injury
  2. Functions of mitochondrial arginase-II in regulation of glucose tolerance and insulin sensitivity in obesity and aging: impact on adipose tissue inflammation, fatty liver, and pancreatic insulin production.
  3. Functions of mitochondrial arginase-II in water balance, inflammaging, and fibrosis in aging kidney.
  4. Roles of mitochondrial arginase-II in melanoma cell proliferation and metastasis.
  5. Signaling transduction mechanisms mediating cell proliferation, cell death, autophagy, and cellular senescence in aging models.