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The use of thiazolidinediones, drugs for type 2 diabetes that may also be useful for other chronic inflammatory disorders, is limited by fluid retention. Research in mice identifies a mechanism for this side effect and introduces a potential remedy (pages 861–866).
The future of cancer treatment lies in targeted therapies. That oft-repeated phrase of the last few years comes with a warning: watch out for drug resistance. A new mathematical model explores how combinations of drugs could keep resistance at bay.
The buildup of protein aggregates consisting of proteins such as tau, huntingtin and amyloid-β occurs in a range of degenerative disorders. Recent studies have begun to shed light on the relative contribution of aggregates versus other, intermediate forms of the protein to disease. The most recent entry in the field examines the protein tau.
A snarl of regulators influence cardiac hypertrophy, but factors that negatively regulate this process are not well understood. A new molecule has now emerged that seems to control pathologic but not physiologic cardiac hypertrophy in mice. It works by repressing the activity of a key transcription factor after both molecules are induced (pages 837–844).
Two studies show how the enzyme ACE2 protects against lung injury caused by SARS and other agents. ACE2 seems to counteract the effects of ACE, which are more damaging (pages 875–879).
The tyrosine kinase inhibitor Gleevec, currently used to treat cancers such as chronic myeloid leukemia, can also function as an antiviral drug to treat poxvirus infections (pages 731–739).
Inflammatory signals strongly influence the generation of T-cell memory after infection or vaccination. Experimental manipulation of these signals shortens the interval of time between administration of a vaccine and a booster (pages 748–756).
Findings over the last year or so have built the case that microRNAs might contribute to cancer. Three studies now definitively show this to be the case and also suggest that these small RNAs could be used to categorize tumors.
Autoimmune processes that destroy insulin-producing cells in the pancreas cause type 1 diabetes. To prevent the disease, autoreactive immune cells need to be suppressed or eliminated without deleterious side effects. Results from a phase 2 clinical trial take steps in this direction.
New vaccines protect monkeys from Ebola and Marburg virus infections after a single shot. The live vaccines are built using a virus platform that should allow widespread protection in people, if the approach holds up in later safety and efficacy studies (pages 786–790).
Genome instability and DNA repair defects have been discovered in the premature aging disease Hutchinson-Gilford progeria syndrome. These findings provide the first hint of a molecular mechanism for a group of human conditions caused by defects in the nuclear structural protein lamin A (pages 780–785).
PPARα reduces fat accumulation and enhances insulin sensitivity, but exactly how it operates has been unclear. Work on mice suggests that newly synthesized fat—but not preexisting fat—activates this transcription factor.
Fish oil has anti-inflammatory properties, but for years the mechanism has remained obscure. That mechanism now begins to come to light—and aspirin may feed into the system by promoting the production of lipid mediators derived from the oil.
The theory that oxidative stress limits lifespan and causes age-related disease rests on experiments in invertebrates and correlative evidence from studies in mammals. This theory now gains a strong experimental basis in mammals.
